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        <title>Am J Physiol Heart C... via MedWorm.com</title>
        <description>MedWorm.com provides a medical RSS filtering service. Over 6000 RSS medical sources are combined and output via different filters. This feed contains the latest items from the 'Am J Physiol Heart C...' source.</description>
        <link><![CDATA[http://www.medworm.com/rss/search.php?qu=Am+J+Physiol+Heart+C...&t=Am+J+Physiol+Heart+C...&s=Search&f=source]]></link>
        <lastBuildDate>Mon, 15 Mar 2010 13:59:32 +0100</lastBuildDate>
        <item>
            <title>Am J Physiol Heart Circ Physiol; +36 new citations</title>
            <link>http://www.medworm.com/index.php?rid=3288433&amp;cid=s_29164_7_f&amp;fid=29164&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fsites%2Fentrez%3Fcmd%3DSearch%26db%3Dpubmed%26term%3D%28%28%28Am%2520J%2520Physiol%2520Heart%2520Circ%2520Physiol%29%2520AND%2520%25222010%252F02%252F17%252020.30%2522%255BMHDA%255D%253A%25222010%252F02%252F19%252017.22%2522%255BMHDA%255D%29%29%2520NOT%2520%28%28%2520%28%28%28%2522Am%2520J%2520Physiol%2520Heart%2520Circ%2520Physiol%2522%255BTIAB%255D%29%29%29%2520AND%2520%25220001%2522%255BEDAT%255D%253A%25222010%252F02%252F17%252020.30%2522%255BEDAT%255D%29%29</link>
            <description>36 new pubmed citations were retrieved for your search.
Click on the search hyperlink below to display the complete search results:

Am J Physiol Heart Circ Physiol
These pubmed results were generated on 2010/02/19PubMed, a service of the National Library of Medicine, includes over 15 million 
citations for biomedical articles back to the 1950's.
These citations are from MEDLINE and additional life science journals. 
PubMed includes links to many sites providing full text articles and other related resources. (Source: Am J Physiol Heart C...)</description>
            <author>Am J Physiol Heart C...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3288433</comments>
            <pubDate>Fri, 19 Feb 2010 22:22:03 +0100</pubDate>
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        <item>
            <title>Am J Physiol Heart Circ Physiol; +62 new citations</title>
            <link>http://www.medworm.com/index.php?rid=3280556&amp;cid=s_29164_7_f&amp;fid=29164&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fsites%2Fentrez%3Fcmd%3DSearch%26db%3Dpubmed%26term%3D%28%28%28Am%2520J%2520Physiol%2520Heart%2520Circ%2520Physiol%29%2520AND%2520%25222010%252F02%252F10%252009.02%2522%255BMHDA%255D%253A%25222010%252F02%252F17%252020.30%2522%255BMHDA%255D%29%29%2520NOT%2520%28%28%2520%28%28%28%2522Am%2520J%2520Physiol%2520Heart%2520Circ%2520Physiol%2522%255BTIAB%255D%29%29%29%2520AND%2520%25220001%2522%255BEDAT%255D%253A%25222010%252F02%252F10%252009.02%2522%255BEDAT%255D%29%29</link>
            <description>62 new pubmed citations were retrieved for your search.
Click on the search hyperlink below to display the complete search results:

Am J Physiol Heart Circ Physiol
These pubmed results were generated on 2010/02/17PubMed, a service of the National Library of Medicine, includes over 15 million 
citations for biomedical articles back to the 1950's.
These citations are from MEDLINE and additional life science journals. 
PubMed includes links to many sites providing full text articles and other related resources. (Source: Am J Physiol Heart C...)</description>
            <author>Am J Physiol Heart C...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3280556</comments>
            <pubDate>Thu, 18 Feb 2010 01:30:02 +0100</pubDate>
            <guid isPermaLink="false">3280556</guid>        </item>
        <item>
            <title>Letter to the editor: &quot;Postulated functional advantages of a looped as opposed to a linearly arranged heart&quot;.</title>
            <link>http://www.medworm.com/index.php?rid=3198154&amp;cid=s_29164_7_f&amp;fid=29164&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20090009%26dopt%3DAbstract</link>
            <description>Authors: Kilner PJ
    
    PMID: 20090009 [PubMed - in process] (Source: Am J Physiol Heart C...)</description>
            <author>Am J Physiol Heart C...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3198154</comments>
            <pubDate>Fri, 22 Jan 2010 22:16:07 +0100</pubDate>
            <guid isPermaLink="false">3198154</guid>        </item>
        <item>
            <title>Letter to the editor: &quot;Depolarization and repolarization alternans in an anesthetized canine ischemia model&quot;.</title>
            <link>http://www.medworm.com/index.php?rid=3198153&amp;cid=s_29164_7_f&amp;fid=29164&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20090011%26dopt%3DAbstract</link>
            <description>Authors: Madias JE
    
    PMID: 20090011 [PubMed - in process] (Source: Am J Physiol Heart C...)</description>
            <author>Am J Physiol Heart C...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3198153</comments>
            <pubDate>Fri, 22 Jan 2010 22:16:05 +0100</pubDate>
            <guid isPermaLink="false">3198153</guid>        </item>
        <item>
            <title>Am J Physiol Heart Circ Physiol; +35 new citations</title>
            <link>http://www.medworm.com/index.php?rid=3149667&amp;cid=s_29164_7_f&amp;fid=29164&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fsites%2Fentrez%3Fcmd%3DSearch%26db%3Dpubmed%26term%3D%28%28%28Am%2520J%2520Physiol%2520Heart%2520Circ%2520Physiol%29%2520AND%2520%25222010%252F01%252F02%252006.32%2522%255BMHDA%255D%253A%25222010%252F01%252F07%252020.12%2522%255BMHDA%255D%29%29%2520NOT%2520%28%28%2520%28%28%28%2522Am%2520J%2520Physiol%2520Heart%2520Circ%2520Physiol%2522%255BTIAB%255D%29%29%29%2520AND%2520%25220001%2522%255BEDAT%255D%253A%25222010%252F01%252F02%252006.32%2522%255BEDAT%255D%29%29</link>
            <description>35 new pubmed citations were retrieved for your search.
Click on the search hyperlink below to display the complete search results:

Am J Physiol Heart Circ Physiol
These pubmed results were generated on 2010/01/07PubMed, a service of the National Library of Medicine, includes over 15 million 
citations for biomedical articles back to the 1950's.
These citations are from MEDLINE and additional life science journals. 
PubMed includes links to many sites providing full text articles and other related resources. (Source: Am J Physiol Heart C...)</description>
            <author>Am J Physiol Heart C...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3149667</comments>
            <pubDate>Fri, 08 Jan 2010 01:12:02 +0100</pubDate>
            <guid isPermaLink="false">3149667</guid>        </item>
        <item>
            <title>Lysophosphatidic acid induces interleukin 6 secretion from aortic smooth muscle cells via an LPA1-regulated, PKC-dependent and p38{alpha}-mediated pathway.</title>
            <link>http://www.medworm.com/index.php?rid=3136123&amp;cid=s_29164_7_f&amp;fid=29164&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20044439%26dopt%3DAbstract</link>
            <description>Authors: Hao F, Tan M, Wu DD, Xu X, Cui MZ
    Lysophosphatidic acid (LPA) is a potent bioactive lysophospholipid. Accumulated evidence supports a role of LPA in inflammation. To profile LPA-induced cytokine production in vascular smooth muscle cells (SMC), we used a cytokine antibody array system and found that LPA prominently induces the secretion of interleukin 6 (IL-6) and monocyte chemoattractant protein-1 (MCP-1) from human aortic smooth muscle cells (HASMCs). The mechanism by which LPA induces MCP-1 expression in SMCs has been reported previously. However, LPA induction of IL-6 secretion from vascular SMCs and its regulatory mechanism are unknown. The present study reveals that LPA induces the expression of IL-6 mRNA and protein in HASMC as well as the secretion of IL-6 protein in a...</description>
            <author>Am J Physiol Heart C...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3136123</comments>
            <pubDate>Thu, 31 Dec 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3136123</guid>        </item>
        <item>
            <title>Contribution of BKCa channels to local metabolic coronary vasodilation: Effects of metabolic syndrome.</title>
            <link>http://www.medworm.com/index.php?rid=3136122&amp;cid=s_29164_7_f&amp;fid=29164&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20044440%26dopt%3DAbstract</link>
            <description>Authors: Borbouse L, Dick GM, Payne GA, Payne BD, Svendsen MC, Neeb ZP, Alloosh M, Bratz IN, Sturek M, Tune JD
    This investigation was designed to examine the hypothesis that impaired function of coronary microvascular BKCa channels in metabolic syndrome (MetS) significantly attenuates the balance between myocardial oxygen delivery and metabolism at rest and during exercise-induced increases in myocardial oxygen consumption (MVO2). Studies were conducted in conscious, chronically instrumented Ossabaw swine fed a normal maintenance diet (11% kcal from fat) or an excess calorie atherogenic diet (43% kcal from fat, 2% cholesterol, 20% kcal from fructose) that induces many common features of MetS. Data were collected under baseline/resting conditions and during graded treadmill exercise bef...</description>
            <author>Am J Physiol Heart C...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3136122</comments>
            <pubDate>Thu, 31 Dec 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3136122</guid>        </item>
        <item>
            <title>Hemoglobin encapsulation in vesicles retards NO- and CO-binding and O2-release when perfused through narrow gas-permeable tubes.</title>
            <link>http://www.medworm.com/index.php?rid=3136121&amp;cid=s_29164_7_f&amp;fid=29164&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20044441%26dopt%3DAbstract</link>
            <description>We examined these gas reactions when Hb-containing solutions of four kinds were perfused through artificial narrow tubes at a practical Hb concentration (10 g/dL). Purified Hb solution, polymerized bovine Hb (PolyBHb), encapsulated Hb (Hb-vesicles, HbV, 279 nm), and RBCs were perfused through a gas-permeable narrow tube (25 microm inner diameter) at 1 mm/s centerline velocity. The level of reactions was determined microscopically based on he visible-light absorption spectrum of Hb. When the tube was immersed in NO and CO atmospheres, both NO-binding and CO-binding of deoxygenated Hb and PolyBHb in the tube were faster than those of HbV and RBCs, and HbV and RBCs showed almost identical binding rates. When the tube was immersed in a N2 atmosphere, oxygenated Hb and PolyBHb showed much faste...</description>
            <author>Am J Physiol Heart C...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3136121</comments>
            <pubDate>Thu, 31 Dec 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3136121</guid>        </item>
        <item>
            <title>Immune regulation and vascular inflammation in genetic hypertension.</title>
            <link>http://www.medworm.com/index.php?rid=3136120&amp;cid=s_29164_7_f&amp;fid=29164&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20044442%26dopt%3DAbstract</link>
            <description>IMMUNE REGULATION AND VASCULAR INFLAMMATION IN GENETIC HYPERTENSION.
    Am J Physiol Heart Circ Physiol. 2009 Dec 31;
    Authors: Viel EC, Lemari&amp;#xE9; CA, Benkirane K, Paradis P, Schiffrin EL
    Immune cells have been implicated in the pathogenesis of hypertension. We hypothesized that under the influence of chromosome 2 (chr2), T lymphocytes contribute to vascular inflammation in genetic salt-sensitive hypertension. Normotensive (Brown Norway), hypertensive (Dahl salt-sensitive) and consomic rats (SSBN2, in which chr2 has been transferred from Brown Norway to Dahl rats) were studied. Systolic blood pressure measured by tail-cuff and aortic preproendothelin mRNA measured by RT-qPCR were elevated in Dahl rats compared with Brown Norway rats, and were reduced in SSBN2 compared with Dahl ...</description>
            <author>Am J Physiol Heart C...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3136120</comments>
            <pubDate>Thu, 31 Dec 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3136120</guid>        </item>
        <item>
            <title>Chronic Physical Activity Mitigates Cerebral Hypoperfusion during Central Hypovolemia in Elderly Humans.</title>
            <link>http://www.medworm.com/index.php?rid=3136119&amp;cid=s_29164_7_f&amp;fid=29164&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20044443%26dopt%3DAbstract</link>
            <description>This study sought to test the hypothesis that orthostasis-induced cerebral hypoperfusion would be less severe in physically active (ACT) than in sedentary (SED) elderly humans. Peak O2 uptake of 10 SED (67.1+/-1.4 yr) and 9 ACT (68.0+/-1.1 yr) volunteers was determined by a graded cycling exercise test (22.1+/-1.2 vs 35.8+/-1.3 ml/min/kg, P&amp;lt;0.01). Baseline mean arterial pressure (MAP, Tonometry) and middle cerebral arterial blood flow velocity (VMCA, transcranial Doppler) were similar between the groups (SED vs ACT: 91+/-3 vs 87+/-3 mmHg and 54.9+/-2.3 vs 57.8+/-3.2 cm/s, respectively); whereas heart rate was higher and stroke volume (Bio-Impedance) was smaller in SED than in ACT. Central hypovolemia during graded lower body negative pressure (LBNP) was larger (P&amp;lt;0.01) in ACT than in...</description>
            <author>Am J Physiol Heart C...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3136119</comments>
            <pubDate>Thu, 31 Dec 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3136119</guid>        </item>
        <item>
            <title>Down Regulated Kv4.3 Expression in the RVLM as a Potential Mechanism of Sympatho-Excitation in Chronic Heart Failure Rats.</title>
            <link>http://www.medworm.com/index.php?rid=3136118&amp;cid=s_29164_7_f&amp;fid=29164&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20044444%26dopt%3DAbstract</link>
            <description>Authors: Gao L, Li Y, Schultz HD, Wang WZ, Wang W, Finch M, Smith LM, Zucker IH
    Elevated central Angiotensin II (Ang II) plays a critical role in the sympatho-excitation of chronic heart failure (CHF) by stimulating up-regulated Angiotensin type 1 receptors (AT1R) in the rostral ventrolateral medulla (RVLM). However, the link between Ang II signaling and electrophysiological characteristics of neurons in the RVLM remains unclear. In the present experiments, we screened for potentially altered genes in the medulla of rats with CHF that are directly related to neuronal membrane conductance using the Rat Genome 230 2.0 Array GeneChip. We found that CHF rats exhibited a 2.1-fold reduction in Kv4.3 gene expression, one of the main voltage-gated K(+) channels, in the medulla. Real-time RT-PC...</description>
            <author>Am J Physiol Heart C...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3136118</comments>
            <pubDate>Thu, 31 Dec 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3136118</guid>        </item>
        <item>
            <title>Nitroglycerin-induced preconditioning: interaction with nitrate tolerance.</title>
            <link>http://www.medworm.com/index.php?rid=3099518&amp;cid=s_29164_7_f&amp;fid=29164&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20008266%26dopt%3DAbstract</link>
            <description>Authors: Csont T
    none Key words: nitroglycerin, preconditioning, endothelial dysfunction, nitrate tolerance.
    PMID: 20008266 [PubMed - as supplied by publisher] (Source: Am J Physiol Heart C...)</description>
            <author>Am J Physiol Heart C...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3099518</comments>
            <pubDate>Fri, 11 Dec 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3099518</guid>        </item>
        <item>
            <title>Protein Kinases A and C Regulate Receptor-Mediated Increases in cAMP in Rabbit Erythrocytes.</title>
            <link>http://www.medworm.com/index.php?rid=3099517&amp;cid=s_29164_7_f&amp;fid=29164&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20008267%26dopt%3DAbstract</link>
            <description>Authors: Adderley SP, Sridharan M, Bowles EA, Stephenson AH, Ellsworth ML, Sprague RS
    Activation of the beta-adrenergic receptor (betaAR) or the prostacyclin receptor (IPR) results in increases in cAMP and ATP release from erythrocytes. cAMP levels depend on a balance between synthesis via adenylyl cyclase and hydrolysis by phosphodiesterases (PDEs). Previously we reported that cAMP increases associated with activation of the betaAR and IPR in rabbit and human erythrocytes are tightly regulated by distinct PDEs. Importantly, inhibitors of these PDEs potentiated both increases in cAMP and ATP release. It has been shown that increases in protein kinase (PK) activity can activate PDEs 3 and 4. Both PKA and PKC are present in the erythrocyte and can phosphorylate and activate these PDEs. H...</description>
            <author>Am J Physiol Heart C...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3099517</comments>
            <pubDate>Fri, 11 Dec 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3099517</guid>        </item>
        <item>
            <title>Chronic Urotensin-II infusion induces diastolic dysfunction and enhances collagen production in rats.</title>
            <link>http://www.medworm.com/index.php?rid=3099516&amp;cid=s_29164_7_f&amp;fid=29164&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20008268%26dopt%3DAbstract</link>
            <description>Conclusion: Chronic U-II infusion causes diastolic dysfunction, caused by fibrosis of the LV. The in vitro data suggests that this may be in part occurring via a ROCK dependent pathway. Key words: Cardiac Remodeling, Rho Kinase, Fibrosis, Urotensin II.
    PMID: 20008268 [PubMed - as supplied by publisher] (Source: Am J Physiol Heart C...)</description>
            <author>Am J Physiol Heart C...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3099516</comments>
            <pubDate>Fri, 11 Dec 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3099516</guid>        </item>
        <item>
            <title>Diabetic Conditions Promote Binding of Monocytes to Vascular Smooth Muscle Cells and their Subsequent Differentiation.</title>
            <link>http://www.medworm.com/index.php?rid=3099515&amp;cid=s_29164_7_f&amp;fid=29164&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20008269%26dopt%3DAbstract</link>
            <description>We examined the hypothesis that enhanced monocyte/vascular smooth muscle cell (VSMC) interactions leading to subendothelial monocyte retention and differentiation to macrophages under diabetic conditions may be underlying mechanisms. Human aortic VSMCs (HVSMCs) treated with diabetic stimuli high glucose (HG) or S100B, a ligand of the receptor for advanced glycation end products, exhibited significantly increased binding of THP-1 monocytic cells. Diabetic stimuli increased the expression of the adhesive chemokine fractalkaline (FKN) in HVSMCs. Pretreatment of HVSMCs with FKN or monocyte chemoattractant protein-1 (MCP-1) neutralizing antibodies significantly inhibited monocyte-VSMC binding, while monocytes treated with FKN showed enhanced binding to VSMC. Mouse aortic VSMCs (MVSMCs) derived ...</description>
            <author>Am J Physiol Heart C...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3099515</comments>
            <pubDate>Fri, 11 Dec 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3099515</guid>        </item>
        <item>
            <title>Baroreflex control of muscle sympathetic nerve activity: a non-pharmacological measure of baroreflex sensitivity.</title>
            <link>http://www.medworm.com/index.php?rid=3099514&amp;cid=s_29164_7_f&amp;fid=29164&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20008270%26dopt%3DAbstract</link>
            <description>BAROREFLEX CONTROL OF MUSCLE SYMPATHETIC NERVE ACTIVITY: A NON-PHARMACOLOGICAL MEASURE OF BAROREFLEX SENSITIVITY.
    Am J Physiol Heart Circ Physiol. 2009 Dec 11;
    Authors: Hart EC, Joyner MJ, Wallin BG, Karlsson T, Curry TB, Charkoudian N
    The sensitivity of baroreflex control of sympathetic nerve activity (SNA) represents the responsiveness of SNA to changes in blood pressure. In a slightly different analysis, the baroreflex threshold measures the probability of whether a sympathetic burst will occur at a given diastolic blood pressure. We hypothesized that baroreflex threshold analysis could be used to estimate the sensitivity of the sympathetic baroreflex measured by the pharmacological modified Oxford test. We compared four measures of sympathetic baroreflex sensitivity in 25 y...</description>
            <author>Am J Physiol Heart C...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3099514</comments>
            <pubDate>Fri, 11 Dec 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3099514</guid>        </item>
        <item>
            <title>Phospholemman and {beta}-adrenergic stimulation in the heart.</title>
            <link>http://www.medworm.com/index.php?rid=3099513&amp;cid=s_29164_7_f&amp;fid=29164&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20008271%26dopt%3DAbstract</link>
            <description>Authors: Wang J, Gao E, Song J, Zhang XQ, Li J, Koch WJ, Tucker AL, Philipson KD, Chan TO, Feldman AM, Cheung JY
    Phosphorylation at serine(68) of phospholemman (PLM) in response to beta-adrenergic stimulation results in simultaneous inhibition of cardiac Na(+)/Ca(2+) exchanger (NCX1) and relief of inhibition of Na(+)-K(+)-ATPase. The role of PLM in mediating beta-adrenergic effects on in vivo cardiac function was investigated using congenic PLM knockout (KO) mice. Echocardiography showed similar ejection fraction between wild-type (WT) and PLM-KO hearts. Cardiac catheterization demonstrated higher baseline contractility (+dP/dt) but similar relaxation (-dP/dt) in PLM-KO mice. In response to isoproterenol (Iso), maximal +dP/dt was similar but maximal -dP/dt was reduced in PLM-KO mice. T...</description>
            <author>Am J Physiol Heart C...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3099513</comments>
            <pubDate>Fri, 11 Dec 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3099513</guid>        </item>
        <item>
            <title>The arterial reservoir pressure increases with aging and is the major determinant of the aortic augmentation index.</title>
            <link>http://www.medworm.com/index.php?rid=3099512&amp;cid=s_29164_7_f&amp;fid=29164&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20008272%26dopt%3DAbstract</link>
            <description>In conclusion, augmentation index is principally determined by aortic reservoir function and other elastic arteries and only to a minor extent by reflected waves. Reservoir function rather than wave reflection changes markedly with aging, which accounts for the age-related changes in the aortic pressure waveform. Key words: arteries, blood pressure, ageing.
    PMID: 20008272 [PubMed - as supplied by publisher] (Source: Am J Physiol Heart C...)</description>
            <author>Am J Physiol Heart C...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3099512</comments>
            <pubDate>Fri, 11 Dec 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3099512</guid>        </item>
        <item>
            <title>Involvement of calcium-calmodulin dependent protein kinase II in endothelin receptor expression in rat cerebral arteries.</title>
            <link>http://www.medworm.com/index.php?rid=3099511&amp;cid=s_29164_7_f&amp;fid=29164&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20008273%26dopt%3DAbstract</link>
            <description>Authors: Waldsee R, Ahnstedt H, Eftekhari S, Edvinsson L
    Experimental cerebral ischemia and organ culture of cerebral arteries result in the enhanced expression of endothelin ETB receptors in smooth muscle cells via increased transcription. The present study was designed to evaluate the involvement of calcium-calmodulin-dependent protein kinase (CAMK) in the transcriptional expression of endothelin receptors after organ culture. Rat basilar arteries were incubated for 24 hours with or without the CAMK inhibitor KN93 or ERK1/2 inhibitor U0126. The contractile responses to endothelin-1 (ET-1; ETA and ETB receptor agonist) and sarafotoxin 6c (S6c; ETB receptor agonist) were studied using a sensitive myograph. The mRNA levels of the ETA and ETB receptors and CAMKII were determined by real-...</description>
            <author>Am J Physiol Heart C...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3099511</comments>
            <pubDate>Fri, 11 Dec 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3099511</guid>        </item>
        <item>
            <title>Gene Expression Profiling of Dilated Cardiomyopathy in Aged Male EP4 Knockout Mice.</title>
            <link>http://www.medworm.com/index.php?rid=3099510&amp;cid=s_29164_7_f&amp;fid=29164&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20008274%26dopt%3DAbstract</link>
            <description>In conclusion, EP4 knockdown in cardiac myocytes in aged male KO mice is in part associated with increased fibrosis, reduced EF and dilated cardiomyopathy. Early overexpression of GDF-15 in hearts of male KO mice may contribute to or be a marker of the disease phenotype. The absence of serious cardiac dysfunction in aged female mice suggests a sexual dimorphism in the phenotype. Key words: heart, gene array, EP4, remodeling.
    PMID: 20008274 [PubMed - as supplied by publisher] (Source: Am J Physiol Heart C...)</description>
            <author>Am J Physiol Heart C...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3099510</comments>
            <pubDate>Fri, 11 Dec 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3099510</guid>        </item>
        <item>
            <title>Autophagy and Protein Kinase C Are Required for Cardioprotection by Sulfaphenazole.</title>
            <link>http://www.medworm.com/index.php?rid=3099509&amp;cid=s_29164_7_f&amp;fid=29164&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20008275%26dopt%3DAbstract</link>
            <description>Authors: Huang C, Liu W, Perry CN, Yitzhaki S, Lee Y, Yuan H, Tsukada YT, Hamacher-Brady A, Mentzer RM, Gottlieb RA
    Previously we showed that sulfaphenazole (SUL), an antimicrobial agent that is a potent inhibitor of cytochrome P4502C9, is protective against ischemia/reperfusion (I/R) injury. The mechanism, however, underlying this cardioprotection, is largely unknown. With evidence that activation of autophagy is protective against simulated I/R in HL-1 cells, and evidence that autophagy is upregulated in preconditioned hearts, we hypothesized that SUL-mediated cardioprotection might resemble ischemic preconditioning with respect to activation of protein kinase C and autophagy. We used the Langendorff model of global ischemia to assess the role of autophagy and protein kinase C in myo...</description>
            <author>Am J Physiol Heart C...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3099509</comments>
            <pubDate>Fri, 11 Dec 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3099509</guid>        </item>
        <item>
            <title>Inhibition of Soluble Epoxide Hydrolase Preserves Cardiomyocytes: Role of STAT3 Signaling.</title>
            <link>http://www.medworm.com/index.php?rid=3099508&amp;cid=s_29164_7_f&amp;fid=29164&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20008276%26dopt%3DAbstract</link>
            <description>Authors: Merkel MJ, Liu L, Cao Z, Packwood WH, Young J, Alkayed NJ, Van Winkle DM
    Soluble epoxide hydrolase (sEH) metabolizes epoxyeicosatrienoic acids (EETs), primarily 14,15-EET. EETs are derived from arachidonic acid via P450 epoxygenases and are cardioprotective. We tested the hypothesis that sEH deficiency and pharmacological inhibition elicit tolerance to ischemia via EET-mediated STAT3 signaling in vitro and in vivo. In addition, the relevance of single nucleotide polymorphisms (SNPs) of EPHX2 (the gene encoding sEH) on tolerance to oxygen/glucose deprivation and reoxygenation/glucose repletion (OGD/RGR) was assessed in male C57BL\6J (WT) or sEH knockout (sEHKO) cardiomyocytes using TAT mediated transduction with sEH mutant proteins. Cell death and hydrolase activity was lower i...</description>
            <author>Am J Physiol Heart C...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3099508</comments>
            <pubDate>Fri, 11 Dec 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3099508</guid>        </item>
        <item>
            <title>Age-dependent Alterations in Fibrillar Collagen Content and Myocardial Diastolic Function: Role of SPARC in Post-Synthetic Procollagen Processing.</title>
            <link>http://www.medworm.com/index.php?rid=3099507&amp;cid=s_29164_7_f&amp;fid=29164&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20008277%26dopt%3DAbstract</link>
            <description>Conclusions: The absence of SPARC reduced age-dependent alterations in ECM fibrillar collagen and diastolic function. These data support the hypothesis that SPARC plays a key role in post-synthetic procollagen processing and contributes to the increase in collagen content found in aged myocardium. Key words: Collagen, SPARC, Aging, Diastolic function.
    PMID: 20008277 [PubMed - as supplied by publisher] (Source: Am J Physiol Heart C...)</description>
            <author>Am J Physiol Heart C...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3099507</comments>
            <pubDate>Fri, 11 Dec 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3099507</guid>        </item>
        <item>
            <title>Resveratrol, an activator of SIRT1 up-regulates sarcoplasmic calcium ATPase and improves cardiac function in diabetic cardiomyopathy.</title>
            <link>http://www.medworm.com/index.php?rid=3099506&amp;cid=s_29164_7_f&amp;fid=29164&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20008278%26dopt%3DAbstract</link>
            <description>This study was designed to examine the effect of Resveratrol (RSV), a potent activator of SIRT1, on cardiac function and SERCA2a expression in chronic type-1 diabetes. Adult male mice were injected with streptozotocin (STZ) and fed with either a regular diet or a diet enriched with RSV. STZ administration produced progressive decline in cardiac function, associated with markedly reduced SERCA2a and SIRT1 protein levels and increased collagen deposition RSV treatment to these mice had a tremendous beneficial effect both in terms of improving SERCA2a expression as well as on cardiac function. In cultured cardiomyocytes RSV restored SERCA2 promoter activity which was otherwise highly repressed in high glucose media. Protective effects of RSV were found dependent on its ability to activate SIR...</description>
            <author>Am J Physiol Heart C...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3099506</comments>
            <pubDate>Fri, 11 Dec 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3099506</guid>        </item>
        <item>
            <title>Am J Physiol Heart Circ Physiol; +17 new citations</title>
            <link>http://www.medworm.com/index.php?rid=3067946&amp;cid=s_29164_7_f&amp;fid=29164&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fsites%2Fentrez%3Fcmd%3DSearch%26db%3Dpubmed%26term%3D%28%28%28Am%2520J%2520Physiol%2520Heart%2520Circ%2520Physiol%29%2520AND%2520%25222009%252F11%252F28%252001.36%2522%255BMHDA%255D%253A%25222009%252F12%252F09%252004.14%2522%255BMHDA%255D%29%29%2520NOT%2520%28%28%2520%28%28%28%2522Am%2520J%2520Physiol%2520Heart%2520Circ%2520Physiol%2522%255BTIAB%255D%29%29%29%2520AND%2520%25220001%2522%255BEDAT%255D%253A%25222009%252F11%252F28%252001.36%2522%255BEDAT%255D%29%29</link>
            <description>17 new pubmed citations were retrieved for your search.
Click on the search hyperlink below to display the complete search results:

Am J Physiol Heart Circ Physiol
These pubmed results were generated on 2009/12/09PubMed, a service of the National Library of Medicine, includes over 15 million 
citations for biomedical articles back to the 1950's.
These citations are from MEDLINE and additional life science journals. 
PubMed includes links to many sites providing full text articles and other related resources. (Source: Am J Physiol Heart C...)</description>
            <author>Am J Physiol Heart C...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3067946</comments>
            <pubDate>Wed, 09 Dec 2009 09:14:02 +0100</pubDate>
            <guid isPermaLink="false">3067946</guid>        </item>
        <item>
            <title>Am J Physiol Heart Circ Physiol; +20 new citations</title>
            <link>http://www.medworm.com/index.php?rid=3034598&amp;cid=s_29164_7_f&amp;fid=29164&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fsites%2Fentrez%3Fcmd%3DSearch%26db%3Dpubmed%26term%3D%28%28%28Am%2520J%2520Physiol%2520Heart%2520Circ%2520Physiol%29%2520AND%2520%25222009%252F11%252F18%252019.14%2522%255BMHDA%255D%253A%25222009%252F11%252F28%252001.36%2522%255BMHDA%255D%29%29%2520NOT%2520%28%28%2520%28%28%28%2522Am%2520J%2520Physiol%2520Heart%2520Circ%2520Physiol%2522%255BTIAB%255D%29%29%29%2520AND%2520%25220001%2522%255BEDAT%255D%253A%25222009%252F11%252F18%252019.14%2522%255BEDAT%255D%29%29</link>
            <description>20 new pubmed citations were retrieved for your search.
Click on the search hyperlink below to display the complete search results:

Am J Physiol Heart Circ Physiol
These pubmed results were generated on 2009/11/28PubMed, a service of the National Library of Medicine, includes over 15 million 
citations for biomedical articles back to the 1950's.
These citations are from MEDLINE and additional life science journals. 
PubMed includes links to many sites providing full text articles and other related resources. (Source: Am J Physiol Heart C...)</description>
            <author>Am J Physiol Heart C...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3034598</comments>
            <pubDate>Sat, 28 Nov 2009 06:36:02 +0100</pubDate>
            <guid isPermaLink="false">3034598</guid>        </item>
        <item>
            <title>Am J Physiol Heart Circ Physiol; +63 new citations</title>
            <link>http://www.medworm.com/index.php?rid=2985779&amp;cid=s_29164_7_f&amp;fid=29164&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fsites%2Fentrez%3Fcmd%3DSearch%26db%3Dpubmed%26term%3D%28%28%28Am%2520J%2520Physiol%2520Heart%2520Circ%2520Physiol%29%2520AND%2520%25222009%252F11%252F05%252020.00%2522%255BMHDA%255D%253A%25222009%252F11%252F13%252006.02%2522%255BMHDA%255D%29%29%2520NOT%2520%28%28%2520%28%28%28%2522Am%2520J%2520Physiol%2520Heart%2520Circ%2520Physiol%2522%255BTIAB%255D%29%29%29%2520AND%2520%25220001%2522%255BEDAT%255D%253A%25222009%252F11%252F05%252020.00%2522%255BEDAT%255D%29%29</link>
            <description>63 new pubmed citations were retrieved for your search.
Click on the search hyperlink below to display the complete search results:

Am J Physiol Heart Circ Physiol
These pubmed results were generated on 2009/11/13PubMed, a service of the National Library of Medicine, includes over 15 million 
citations for biomedical articles back to the 1950's.
These citations are from MEDLINE and additional life science journals. 
PubMed includes links to many sites providing full text articles and other related resources. (Source: Am J Physiol Heart C...)</description>
            <author>Am J Physiol Heart C...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2985779</comments>
            <pubDate>Fri, 13 Nov 2009 11:02:02 +0100</pubDate>
            <guid isPermaLink="false">2985779</guid>        </item>
        <item>
            <title>Am J Physiol Heart Circ Physiol; +17 new citations</title>
            <link>http://www.medworm.com/index.php?rid=2931405&amp;cid=s_29164_7_f&amp;fid=29164&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fsites%2Fentrez%3Fcmd%3DSearch%26db%3Dpubmed%26term%3D%28%28%28Am%2520J%2520Physiol%2520Heart%2520Circ%2520Physiol%29%2520AND%2520%25222009%252F10%252F22%252002.06%2522%255BMHDA%255D%253A%25222009%252F10%252F27%252015.16%2522%255BMHDA%255D%29%29%2520NOT%2520%28%28%2520%28%28%28%2522Am%2520J%2520Physiol%2520Heart%2520Circ%2520Physiol%2522%255BTIAB%255D%29%29%29%2520AND%2520%25220001%2522%255BEDAT%255D%253A%25222009%252F10%252F22%252002.06%2522%255BEDAT%255D%29%29</link>
            <description>17 new pubmed citations were retrieved for your search.
Click on the search hyperlink below to display the complete search results:

Am J Physiol Heart Circ Physiol
These pubmed results were generated on 2009/10/27PubMed, a service of the National Library of Medicine, includes over 15 million 
citations for biomedical articles back to the 1950's.
These citations are from MEDLINE and additional life science journals. 
PubMed includes links to many sites providing full text articles and other related resources. (Source: Am J Physiol Heart C...)</description>
            <author>Am J Physiol Heart C...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2931405</comments>
            <pubDate>Tue, 27 Oct 2009 19:16:02 +0100</pubDate>
            <guid isPermaLink="false">2931405</guid>        </item>
        <item>
            <title>Am J Physiol Heart Circ Physiol; +43 new citations</title>
            <link>http://www.medworm.com/index.php?rid=2880084&amp;cid=s_29164_7_f&amp;fid=29164&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fsites%2Fentrez%3Fcmd%3DSearch%26db%3Dpubmed%26term%3D%28%28%28Am%2520J%2520Physiol%2520Heart%2520Circ%2520Physiol%29%2520AND%2520%25222009%252F10%252F07%252003.22%2522%255BMHDA%255D%253A%25222009%252F10%252F11%252000.16%2522%255BMHDA%255D%29%29%2520NOT%2520%28%28%2520%28%28%28%2522Am%2520J%2520Physiol%2520Heart%2520Circ%2520Physiol%2522%255BTIAB%255D%29%29%29%2520AND%2520%25220001%2522%255BEDAT%255D%253A%25222009%252F10%252F07%252003.22%2522%255BEDAT%255D%29%29</link>
            <description>43 new pubmed citations were retrieved for your search.
Click on the search hyperlink below to display the complete search results:

Am J Physiol Heart Circ Physiol
These pubmed results were generated on 2009/10/11PubMed, a service of the National Library of Medicine, includes over 15 million 
citations for biomedical articles back to the 1950's.
These citations are from MEDLINE and additional life science journals. 
PubMed includes links to many sites providing full text articles and other related resources. (Source: Am J Physiol Heart C...)</description>
            <author>Am J Physiol Heart C...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2880084</comments>
            <pubDate>Sun, 11 Oct 2009 04:16:03 +0100</pubDate>
            <guid isPermaLink="false">2880084</guid>        </item>
        <item>
            <title>Developmental regulation of cardiovascular function is dependent on both genotype and environment.</title>
            <link>http://www.medworm.com/index.php?rid=2842994&amp;cid=s_29164_7_f&amp;fid=29164&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19783772%26dopt%3DAbstract</link>
            <description>DEVELOPMENTAL REGULATION OF CARDIOVASCULAR FUNCTION IS DEPENDENT ON BOTH GENOTYPE AND ENVIRONMENT.
    Am J Physiol Heart Circ Physiol. 2009 Sep 25;
    Authors: Knight BS, Sunn N, Pennell CE, Adamson SL, Lye SJ
    Adverse developmental environments can increase the risk of adult cardiovascular disease but not all individuals are affected, suggesting the importance of genotype. Genetically distinct mouse strains allow genetic dissection of complex-traits; however, they have not been utilized to evaluate the developmental origins of adult cardiovascular disease. Our objective was to determine the effect of prenatal nutrient restriction (R) on adult cardiovascular function in A/J (AJ) and C57BL/6J (B6) mice, and whether postnatal high-fat (HF) diet exacerbates these effects. Pregnant AJ and...</description>
            <author>Am J Physiol Heart C...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2842994</comments>
            <pubDate>Thu, 24 Sep 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2842994</guid>        </item>
        <item>
            <title>Differential Regulation of Vascular Smooth Muscle and Endothelial Cell Proliferation In Vitro and In Vivo by cAMP/PKA-activated p85{alpha}PI3K.</title>
            <link>http://www.medworm.com/index.php?rid=2842993&amp;cid=s_29164_7_f&amp;fid=29164&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19783773%26dopt%3DAbstract</link>
            <description>In conclusions, PKA-activated-p85alpha integrates cAMP/PKA signaling differently in VSMCs and ECs. By reducing neointimal hyperplasia without inhibiting endothelial regeneration, it exerts a protective effect against restenosis after balloon injury. Key words: Restenosis, smooth muscle cells, endothelial cells, cAMP.
    PMID: 19783773 [PubMed - as supplied by publisher] (Source: Am J Physiol Heart C...)</description>
            <author>Am J Physiol Heart C...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2842993</comments>
            <pubDate>Thu, 24 Sep 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2842993</guid>        </item>
        <item>
            <title>Hypersensitivity of excitation-contraction coupling in dystrophic cardiomyocytes.</title>
            <link>http://www.medworm.com/index.php?rid=2842992&amp;cid=s_29164_7_f&amp;fid=29164&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19783774%26dopt%3DAbstract</link>
            <description>Authors: Ullrich ND, Fanchaouy M, Gusev K, Shirokova N, Niggli E
    Duchenne muscular dystrophy represents a severe inherited disease of striated muscle. It is caused by a mutation of the dystrophin gene and characterized by a progressive loss of skeletal muscle function. Most patients also develop a dystrophic cardiomyopathy resulting in dilated hypertrophy and heart failure, but cellular mechanisms leading to deterioration of cardiac function remain elusive. Here we tested whether defective excitation-contraction (EC) coupling contributes to impaired cardiac performance. &quot;EC-coupling gain&quot; was determined in cardiomyocytes from control and dystrophin-deficient mdx mice. To this end, Ca2+ currents (ICaL) were measured with the whole-cell patch-clamp technique, while Ca(2+) transients were...</description>
            <author>Am J Physiol Heart C...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2842992</comments>
            <pubDate>Thu, 24 Sep 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2842992</guid>        </item>
        <item>
            <title>Allogenic stem cell therapy improves right ventricular function by improving lung pathology in rats with pulmonary hypertension.</title>
            <link>http://www.medworm.com/index.php?rid=2842991&amp;cid=s_29164_7_f&amp;fid=29164&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19783775%26dopt%3DAbstract</link>
            <description>Authors: Umar S, de Visser YP, Steendijk P, Schutte CI, Laghmani EH, Wagenaar GT, Bax WH, Mantikou E, Pijnappels DA, Atsma DE, Schalij MJ, van der Wall EE, van der Laarse A
    Pulmonary arterial hypertension (PAH) is a chronic lung disease that leads to right ventricular hypertrophy (RVH), remodeling and failure. We tested treatment with bone marrow-derived mesenchymal stem cells (MSCs) obtained from donor rats with monocrotaline (MCT)-induced PAH to recipient rats with MCT-induced PAH on pulmonary artery pressure, lung pathology and RV function. This model was chosen to mimic autologous MSC therapy. At day 1, PAH was induced by MCT (60 mg/kg) in 20 female Wistar rats. At day 14, rats were treated with 10(6) MSCs i.v. (MCT+MSC) or saline (MCT60). MSCs were obtained from donor rats with PA...</description>
            <author>Am J Physiol Heart C...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2842991</comments>
            <pubDate>Thu, 24 Sep 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2842991</guid>        </item>
        <item>
            <title>Role of nitric oxide as a key mediator on cardiovascular actions of atrial natriuretic peptide in spontaneously hypertensive rats.</title>
            <link>http://www.medworm.com/index.php?rid=2842990&amp;cid=s_29164_7_f&amp;fid=29164&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19783776%26dopt%3DAbstract</link>
            <description>Conclusions: In atria, ventricle and aorta, ANP interacts with NPR-C receptors, activating Ca-calmodulin eNOS through Gi protein. In ventricle and aorta, NOS activation also involves NPR-A/B. NOS response to ANP was impaired in heart and aorta of SHR. Impaired NO-system response to ANP in hypertensive animals, involving alterations in the signaling pathway, could participate in maintenance of high blood pressure in this model of hypertension. Key words: cardiovascular nitric oxide synthase, hypertension, aorta artery, heart.
    PMID: 19783776 [PubMed - as supplied by publisher] (Source: Am J Physiol Heart C...)</description>
            <author>Am J Physiol Heart C...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2842990</comments>
            <pubDate>Thu, 24 Sep 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2842990</guid>        </item>
        <item>
            <title>Additive Beneficial Effects of Lactotripeptide and Aerobic Exercise on Arterial Compliance in Postmenopausal Women.</title>
            <link>http://www.medworm.com/index.php?rid=2842989&amp;cid=s_29164_7_f&amp;fid=29164&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19783777%26dopt%3DAbstract</link>
            <description>Authors: Yoshizawa M, Maeda S, Miyaki A, Misono M, Choi Y, Shimojo N, Ajisaka R, Tanaka H
    Central arterial compliance plays an important role in the functional abilities of the vasculature. Two active tripeptides, valine-proline-proline (Val-Pro-Pro) and isoleucine-Pro-Pro (Ile-Pro-Pro), were isolated from the sour milk and were referred to lactotripeptide (LTP). Because LTP appears to act as angiotensin-converting enzyme (ACE) inhibitor, it is plausible to hypothesize that LTP improves arterial compliance. We determined the effects of LTP ingestion alone or in combination with regular aerobic exercise on arterial compliance. A total of 55 postmenopausal women (50-65 years old) were randomly divided into four groups: placebo, LTP, exercise and placebo (Ex+Placebo), or exercise and LTP ...</description>
            <author>Am J Physiol Heart C...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2842989</comments>
            <pubDate>Thu, 24 Sep 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2842989</guid>        </item>
        <item>
            <title>Structural adaptation of microvessel diameters in response to metabolic stimuli: Where are the oxygen sensors?</title>
            <link>http://www.medworm.com/index.php?rid=2842988&amp;cid=s_29164_7_f&amp;fid=29164&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19783778%26dopt%3DAbstract</link>
            <description>Authors: Reglin B, Secomb TW, Pries AR
    Maintenance of functional vascular networks requires structural adaptation of vessel diameters in response to hemodynamic and metabolic conditions. The mechanisms by which diameters respond to the metabolic state are not known but may involve the release of vasoactive substances in response to low oxygen by tissue (&quot;tissue signaling&quot;, e.g. CO2, adenosine), by vessel walls (&quot;wall signaling&quot;, e.g. prostaglandins, adenosine) and/or by red blood cells, RBCs (&quot;RBC signaling&quot;, e.g. ATP and NO). Here, the goal was to test the potential of each of these locations of oxygen-dependent signaling to control steady-state vascular diameters and tissue oxygenation. A previously developed theoretical model of structural diameter adaptation based on experimental d...</description>
            <author>Am J Physiol Heart C...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2842988</comments>
            <pubDate>Thu, 24 Sep 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2842988</guid>        </item>
        <item>
            <title>Abnormal Nitric Oxide Production in Aged Rat Mesenteric Arteries is Mediated by NAD(P)H Oxidase-derived Peroxide.</title>
            <link>http://www.medworm.com/index.php?rid=2842987&amp;cid=s_29164_7_f&amp;fid=29164&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19783779%26dopt%3DAbstract</link>
            <description>Authors: Zhou X, Bohlen HG, Unthank JL, Miller SJ
    Previous work in our laboratory showed increased basal periarterial NO and H2O2 concentrations in the Spontaneously Hypertensive Rat (SHR), characterized by oxidant stress, as well as impaired flow-mediated NO production that was corrected by reduction of periarterial H2O2. Aging also is associated with an increase in vascular reactive oxygen species (ROS) and results in abnormal vascular function. The current study was designed to assess the role of H2O2 in regulating NO production during vascular aging. In vivo, real-time NO and H2O2 concentrations were measured by microelectrodes in mesenteric arteries of retired breeder (aged; 8-12 mo) and young (2-3 mo) WKY rats under conditions of altered flow. Results in aged rats revealed elevat...</description>
            <author>Am J Physiol Heart C...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2842987</comments>
            <pubDate>Thu, 24 Sep 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2842987</guid>        </item>
        <item>
            <title>An Adaptive Transfer Function for Deriving the Aortic Pressure Waveform from a Peripheral Artery Pressure Waveform.</title>
            <link>http://www.medworm.com/index.php?rid=2842986&amp;cid=s_29164_7_f&amp;fid=29164&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19783780%26dopt%3DAbstract</link>
            <description>Authors: Swamy G, Xu D, Olivier NB, Mukkamala R
    We developed a new technique to mathematically transform a peripheral artery pressure (PAP) waveform distorted by wave reflections into the physiologically more relevant aortic pressure (AP) waveform. First, a transfer function relating PAP to AP is defined in terms of the unknown parameters of a parallel tube model of pressure and flow in the arterial tree. Then, the parameters are estimated from the measured PAP waveform along with a one-time measurement of the wave propagation delay time between the aorta and peripheral artery measurement site (which may be accomplished non-invasively) by exploiting pre-knowledge of aortic flow. Finally, the transfer function with its estimated parameters is applied to the measured waveform so as to de...</description>
            <author>Am J Physiol Heart C...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2842986</comments>
            <pubDate>Thu, 24 Sep 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2842986</guid>        </item>
        <item>
            <title>Altered reactivity to norepinephrine through COX-2 induction by vascular injury in hypercholesterolemic rabbits.</title>
            <link>http://www.medworm.com/index.php?rid=2842985&amp;cid=s_29164_7_f&amp;fid=29164&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19783781%26dopt%3DAbstract</link>
            <description>Authors: Foudi N, Norel X, Rienzo M, Louedec L, Brink C, Michel JB, Back M
    Although long term use of cyclooxygenase (COX)-2 inhibitors may be associated with increased cardiovascular risk, their effects on vascular reactivity in atherosclerosis has remained largely unexplored. The aim of the present study was to evaluate the role of COX-2 induced by an atherosclerotic process, in the local control of vascular tone. New Zealand White rabbits were fed 0.3% cholesterol and subjected to balloon injury of the abdominal aorta. After 2 weeks, the aorta was removed and used for organ bath experiments and immunohistochemistry, and the prostaglandins released were measured using enzyme immunoassays. Hypercholesterolemia and vascular injury significantly increased the thickness of the intimal lay...</description>
            <author>Am J Physiol Heart C...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2842985</comments>
            <pubDate>Thu, 24 Sep 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2842985</guid>        </item>
        <item>
            <title>Angiotensin II Effects on Ischemic Focal Ventricular Tachycardia are Predominantly Mediated Through Myocardial AT2 Receptor.</title>
            <link>http://www.medworm.com/index.php?rid=2842984&amp;cid=s_29164_7_f&amp;fid=29164&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19783782%26dopt%3DAbstract</link>
            <description>Conclusions: AGII promotes only focal, mainly Purkinje ischemic VT. PD, but not losartan, preferentially blocked focal VT, which is likely due to triggered activity due to delayed afterdepolarizations in Purkinje. Key words: angiotensin II, AT2 receptor, focal ventricular tachycardia, triggered activity.
    PMID: 19783782 [PubMed - as supplied by publisher] (Source: Am J Physiol Heart C...)</description>
            <author>Am J Physiol Heart C...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2842984</comments>
            <pubDate>Thu, 24 Sep 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2842984</guid>        </item>
        <item>
            <title>Am J Physiol Heart Circ Physiol; +39 new citations</title>
            <link>http://www.medworm.com/index.php?rid=2815119&amp;cid=s_29164_7_f&amp;fid=29164&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fsites%2Fentrez%3Fcmd%3DSearch%26db%3Dpubmed%26term%3D%28%28%28Am%2520J%2520Physiol%2520Heart%2520Circ%2520Physiol%29%2520AND%2520%25222009%252F09%252F16%252021.34%2522%255BMHDA%255D%253A%25222009%252F09%252F22%252009.50%2522%255BMHDA%255D%29%29%2520NOT%2520%28%28%2520%28%28%28%2522Am%2520J%2520Physiol%2520Heart%2520Circ%2520Physiol%2522%255BTIAB%255D%29%29%29%2520AND%2520%25220001%2522%255BEDAT%255D%253A%25222009%252F09%252F16%252021.34%2522%255BEDAT%255D%29%29</link>
            <description>39 new pubmed citations were retrieved for your search.
Click on the search hyperlink below to display the complete search results:

Am J Physiol Heart Circ Physiol
These pubmed results were generated on 2009/09/22PubMed, a service of the National Library of Medicine, includes over 15 million 
citations for biomedical articles back to the 1950's.
These citations are from MEDLINE and additional life science journals. 
PubMed includes links to many sites providing full text articles and other related resources. (Source: Am J Physiol Heart C...)</description>
            <author>Am J Physiol Heart C...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2815119</comments>
            <pubDate>Tue, 22 Sep 2009 13:50:02 +0100</pubDate>
            <guid isPermaLink="false">2815119</guid>        </item>
        <item>
            <title>Am J Physiol Heart Circ Physiol; +48 new citations</title>
            <link>http://www.medworm.com/index.php?rid=2762625&amp;cid=s_29164_7_f&amp;fid=29164&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fsites%2Fentrez%3Fcmd%3DSearch%26db%3Dpubmed%26term%3D%28%28%28Am%2520J%2520Physiol%2520Heart%2520Circ%2520Physiol%29%2520AND%2520%25222009%252F09%252F02%252004.54%2522%255BMHDA%255D%253A%25222009%252F09%252F04%252000.58%2522%255BMHDA%255D%29%29%2520NOT%2520%28%28%2520%28%28%28%2522Am%2520J%2520Physiol%2520Heart%2520Circ%2520Physiol%2522%255BTIAB%255D%29%29%29%2520AND%2520%25220001%2522%255BEDAT%255D%253A%25222009%252F09%252F02%252004.54%2522%255BEDAT%255D%29%29</link>
            <description>48 new pubmed citations were retrieved for your search.
Click on the search hyperlink below to display the complete search results:

Am J Physiol Heart Circ Physiol
These pubmed results were generated on 2009/09/04PubMed, a service of the National Library of Medicine, includes over 15 million 
citations for biomedical articles back to the 1950's.
These citations are from MEDLINE and additional life science journals. 
PubMed includes links to many sites providing full text articles and other related resources. (Source: Am J Physiol Heart C...)</description>
            <author>Am J Physiol Heart C...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2762625</comments>
            <pubDate>Fri, 04 Sep 2009 04:58:02 +0100</pubDate>
            <guid isPermaLink="false">2762625</guid>        </item>
        <item>
            <title>Nitrite Enhances RBC Hypoxic ATP Synthesis and the Release of ATP into the Vasculature: a new mechanism for nitrite induced vasodilation.</title>
            <link>http://www.medworm.com/index.php?rid=2730932&amp;cid=s_29164_7_f&amp;fid=29164&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19700624%26dopt%3DAbstract</link>
            <description>In this study, we have delineated a mechanism for nitrite induced RBC vasodilation that does not require that NO be released from the cell. Instead we show that nitrite enhances the ATP release from RBCs, which is known to produce vasodilation by several different methods including the interaction with purinergic receptors on the endothelium that stimulate the synthesis of NO by endothelial NO synthase. This mechanism was established in vivo by measuring the decrease in blood pressure when injecting nitrite reacted RBCs into rats. The observed decrease in blood pressure was not observed if e-NOS was inhibited by N-omega-nitro-L-arginine methyl ester (L-NAME) or when any released ATP was degraded by apyrase. The nitrite enhanced ATP release was shown to involve increased binding of nitrite ...</description>
            <author>Am J Physiol Heart C...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2730932</comments>
            <pubDate>Thu, 20 Aug 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2730932</guid>        </item>
        <item>
            <title>Experimental and Theoretical Ventricular Electrograms and their Relation to Electrophysiological Gradients in the Adult Rat Heart.</title>
            <link>http://www.medworm.com/index.php?rid=2730931&amp;cid=s_29164_7_f&amp;fid=29164&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19700625%26dopt%3DAbstract</link>
            <description>In this study, optical mapping techniques have been applied to an in vitro left ventricular adult rat preparation to obtain patterns of conduction and action potential duration measurements from the epicardial surface. This information has been combined with previously published mathematical models of the rat ventricular myocyte to develop a bidomain model for action potential propagation and electrogram formation in the rat left ventricle. Important insights into the basis for the repolarization waveform in the ventricular electrogram of the adult rat have been obtained. Notably, our model demonstrated that the biphasic shape of the rat ventricular repolarization wave can be explained in terms of the transmural and apex-to-base gradients in action potential duration that exist in the rat ...</description>
            <author>Am J Physiol Heart C...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2730931</comments>
            <pubDate>Thu, 20 Aug 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2730931</guid>        </item>
        <item>
            <title>A slowly-inactivating sodium current contributes to spontaneous diastolic depolarization of atrial myocytes.</title>
            <link>http://www.medworm.com/index.php?rid=2730930&amp;cid=s_29164_7_f&amp;fid=29164&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19700626%26dopt%3DAbstract</link>
            <description>In conclusion, late INa can contribute to DD of atrial myocytes, and inhibition of this current suppresses atrial DD and spontaneous APs. Key words: Late sodium current, Atrial myocytes, Diastolic depolarization, Action potential.
    PMID: 19700626 [PubMed - as supplied by publisher] (Source: Am J Physiol Heart C...)</description>
            <author>Am J Physiol Heart C...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2730930</comments>
            <pubDate>Thu, 20 Aug 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2730930</guid>        </item>
        <item>
            <title>Impaired Contractile Function and Calcium Handling in Hearts of Cardiac-specific Calcineurin b1-deficient Mice.</title>
            <link>http://www.medworm.com/index.php?rid=2730929&amp;cid=s_29164_7_f&amp;fid=29164&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19700627%26dopt%3DAbstract</link>
            <description>Authors: Schaeffer PJ, Desantiago J, Yang JH, Flagg TP, Kovacs A, Weinheimer C, Courtois MR, Leone TC, Nichols CG, Bers DM, Kelly DP
    To define the necessity of calcineurin (Cn) signaling for cardiac maturation and function, the postnatal phenotype of mice with cardiac-specific targeted ablation of the Cn B1 regulatory subunit (Ppp3r1) gene (csCnb1(-/-) mice) was characterized. csCnb1(-/-) mice develop a lethal cardiomyopathy characterized by impaired postnatal growth of the heart and combined systolic and diastolic relaxation abnormalities despite a lack of structural derangements. Notably, the csCnb1(-/-) hearts did not exhibit diastolic dilatation despite the severe functional phenotype. Myocytes isolated from the mutant mice exhibited reduced rates of contraction/relaxation and abno...</description>
            <author>Am J Physiol Heart C...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2730929</comments>
            <pubDate>Thu, 20 Aug 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2730929</guid>        </item>
        <item>
            <title>Am J Physiol Heart Circ Physiol; +58 new citations</title>
            <link>http://www.medworm.com/index.php?rid=2700382&amp;cid=s_29164_7_f&amp;fid=29164&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fsites%2Fentrez%3Fcmd%3DSearch%26db%3Dpubmed%26term%3D%28%28%28Am%2520J%2520Physiol%2520Heart%2520Circ%2520Physiol%29%2520AND%2520%25222009%252F08%252F12%252023.16%2522%255BMHDA%255D%253A%25222009%252F08%252F14%252020.14%2522%255BMHDA%255D%29%29%2520NOT%2520%28%28%2520%28%28%28%2522Am%2520J%2520Physiol%2520Heart%2520Circ%2520Physiol%2522%255BTIAB%255D%29%29%29%2520AND%2520%25220001%2522%255BEDAT%255D%253A%25222009%252F08%252F12%252023.16%2522%255BEDAT%255D%29%29</link>
            <description>58 new pubmed citations were retrieved for your search.
Click on the search hyperlink below to display the complete search results:

Am J Physiol Heart Circ Physiol
These pubmed results were generated on 2009/08/14PubMed, a service of the National Library of Medicine, includes over 15 million 
citations for biomedical articles back to the 1950's.
These citations are from MEDLINE and additional life science journals. 
PubMed includes links to many sites providing full text articles and other related resources. (Source: Am J Physiol Heart C...)</description>
            <author>Am J Physiol Heart C...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2700382</comments>
            <pubDate>Sat, 15 Aug 2009 00:14:01 +0100</pubDate>
            <guid isPermaLink="false">2700382</guid>        </item>
        <item>
            <title>Am J Physiol Heart Circ Physiol; +16 new citations</title>
            <link>http://www.medworm.com/index.php?rid=2692638&amp;cid=s_29164_7_f&amp;fid=29164&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fsites%2Fentrez%3Fcmd%3DSearch%26db%3Dpubmed%26term%3D%28%28%28Am%2520J%2520Physiol%2520Heart%2520Circ%2520Physiol%29%2520AND%2520%25222009%252F08%252F05%252014.10%2522%255BMHDA%255D%253A%25222009%252F08%252F12%252023.16%2522%255BMHDA%255D%29%29%2520NOT%2520%28%28%2520%28%28%28%2522Am%2520J%2520Physiol%2520Heart%2520Circ%2520Physiol%2522%255BTIAB%255D%29%29%29%2520AND%2520%25220001%2522%255BEDAT%255D%253A%25222009%252F08%252F05%252014.10%2522%255BEDAT%255D%29%29</link>
            <description>16 new pubmed citations were retrieved for your search.
Click on the search hyperlink below to display the complete search results:

Am J Physiol Heart Circ Physiol
These pubmed results were generated on 2009/08/12PubMed, a service of the National Library of Medicine, includes over 15 million 
citations for biomedical articles back to the 1950's.
These citations are from MEDLINE and additional life science journals. 
PubMed includes links to many sites providing full text articles and other related resources. (Source: Am J Physiol Heart C...)</description>
            <author>Am J Physiol Heart C...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2692638</comments>
            <pubDate>Thu, 13 Aug 2009 03:16:02 +0100</pubDate>
            <guid isPermaLink="false">2692638</guid>        </item>
        <item>
            <title>Interleukin-1{alpha} Stimulates Pro-inflammatory Cytokine Expression in Human Cardiac Myofibroblasts.</title>
            <link>http://www.medworm.com/index.php?rid=2671498&amp;cid=s_29164_7_f&amp;fid=29164&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19648252%26dopt%3DAbstract</link>
            <description>In conclusion, IL-1alpha stimulates human CMF to express IL-1beta, TNFalpha and IL-6 via specific signaling pathways; responses that are unaffected by IL-10 exposure. Key words: cardiac fibroblasts, inflammation, signal transduction, cytokines.
    PMID: 19648252 [PubMed - as supplied by publisher] (Source: Am J Physiol Heart C...)</description>
            <author>Am J Physiol Heart C...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2671498</comments>
            <pubDate>Thu, 30 Jul 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2671498</guid>        </item>
        <item>
            <title>Sphingosine 1-Phosphate is an Important Endogenous Cardioprtectant Released by Ischemic Pre- and Post-Conditioning.</title>
            <link>http://www.medworm.com/index.php?rid=2671497&amp;cid=s_29164_7_f&amp;fid=29164&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19648253%26dopt%3DAbstract</link>
            <description>Authors: Vessey DA, Li L, Honbo N, Karliner JS
    Exogenous sphingosine 1-phosphate (S1P) is an effective cardioprotectant against ischemic injury. We have investigated the hypothesis that S1P is also an important endogenous cardioprotectant released during both ischemic preconditioning (IPC) and ischemic postconditioning (IPOST). IPC of ex vivo rat hearts was instituted by 2 cycles of 3 min ischemia/5 min reperfusion prior to 40 min of index ischemia and then 40 min of reperfusion. IPC resulted in 70% recovery of left ventricular developed pressure (LVDP) upon reperfusion and a small infarct size (10%). VPC23019 (VPC), a specific antagonist of S1P1 and 3 G-protein coupled receptors (GPCRs), when present during preconditioning blocked protection afforded by 2 cycles of IPC. VPC also block...</description>
            <author>Am J Physiol Heart C...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2671497</comments>
            <pubDate>Thu, 30 Jul 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2671497</guid>        </item>
        <item>
            <title>Impact of ionic current variability on human ventricular cellular electrophysiology.</title>
            <link>http://www.medworm.com/index.php?rid=2671496&amp;cid=s_29164_7_f&amp;fid=29164&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19648254%26dopt%3DAbstract</link>
            <description>This study provides quantitative insights into the sensitivity of preclinical biomarkers of arrhythmic risk to variations in ionic current properties in humans. Results show the importance of sensitivity analysis as a powerful method for in depth validation of mathematical models in cardiac electrophysiology. Key words: ionic current, biological variability, arrhythmia, computer simulation.
    PMID: 19648254 [PubMed - as supplied by publisher] (Source: Am J Physiol Heart C...)</description>
            <author>Am J Physiol Heart C...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2671496</comments>
            <pubDate>Thu, 30 Jul 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2671496</guid>        </item>
        <item>
            <title>Autonomic effects on the spectral analysis of heart rate variability after exercise.</title>
            <link>http://www.medworm.com/index.php?rid=2671495&amp;cid=s_29164_7_f&amp;fid=29164&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19648255%26dopt%3DAbstract</link>
            <description>Authors: Ng J, Sundaram S, Kadish AH, Goldberger JJ
    Although frequency domain analysis of heart rate variability (HRV) has been performed in the setting of exercise and recovery from exercise, the relationship of specific frequency components to sympathetic and parasympathetic inputs has not been validated in this setting. The aim of this study is to evaluate the relationship of frequency components of HRV to sympathetic and parasympathetic modulation in the setting of recovery after exercise using selective autonomic blockade. Normal subjects (N=27, 17 male, 53+/-7 years old) underwent bicycle stress testing on four separate days. On Day 1, a baseline study without autonomic blockade was performed. On Days 2 through 4, either beta-adrenergic, parasympathetic, or double blockade was ad...</description>
            <author>Am J Physiol Heart C...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2671495</comments>
            <pubDate>Thu, 30 Jul 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2671495</guid>        </item>
        <item>
            <title>Spontaneous calcium release in tissue from the failing canine heart.</title>
            <link>http://www.medworm.com/index.php?rid=2671494&amp;cid=s_29164_7_f&amp;fid=29164&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19648256%26dopt%3DAbstract</link>
            <description>Conclusions: TA in HF tissue is associated with abnormal calcium regulation and mediated by the spontaneous release of calcium from the SR in aggregates of myocardial cells (i.e. an SCR), but importantly it is the rate of SCR rise rather than amplitude that was associated with TA. Key words: heart failure, arrhythmia, spontaneous calcium release, delayed afterdepolarization.
    PMID: 19648256 [PubMed - as supplied by publisher] (Source: Am J Physiol Heart C...)</description>
            <author>Am J Physiol Heart C...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2671494</comments>
            <pubDate>Thu, 30 Jul 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2671494</guid>        </item>
        <item>
            <title>Am J Physiol Heart Circ Physiol; +36 new citations</title>
            <link>http://www.medworm.com/index.php?rid=2615774&amp;cid=s_29164_7_f&amp;fid=29164&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fsites%2Fentrez%3Fcmd%3DSearch%26db%3Dpubmed%26term%3D%28%28%28Am%2520J%2520Physiol%2520Heart%2520Circ%2520Physiol%29%2520AND%2520%25222009%252F07%252F14%252010.42%2522%255BMHDA%255D%253A%25222009%252F07%252F19%252023.38%2522%255BMHDA%255D%29%29%2520NOT%2520%28%28%2520%28%28%28%2522Am%2520J%2520Physiol%2520Heart%2520Circ%2520Physiol%2522%255BTIAB%255D%29%29%29%2520AND%2520%25220001%2522%255BEDAT%255D%253A%25222009%252F07%252F14%252010.42%2522%255BEDAT%255D%29%29</link>
            <description>36 new pubmed citations were retrieved for your search.
Click on the search hyperlink below to display the complete search results:

Am J Physiol Heart Circ Physiol
These pubmed results were generated on 2009/07/19PubMed, a service of the National Library of Medicine, includes over 15 million 
citations for biomedical articles back to the 1950's.
These citations are from MEDLINE and additional life science journals. 
PubMed includes links to many sites providing full text articles and other related resources. (Source: Am J Physiol Heart C...)</description>
            <author>Am J Physiol Heart C...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2615774</comments>
            <pubDate>Mon, 20 Jul 2009 03:38:02 +0100</pubDate>
            <guid isPermaLink="false">2615774</guid>        </item>
        <item>
            <title>Determinants of left ventricular shear strain.</title>
            <link>http://www.medworm.com/index.php?rid=2598668&amp;cid=s_29164_7_f&amp;fid=29164&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19592607%26dopt%3DAbstract</link>
            <description>In this study, we used a finite element model of left ventricular (LV) mechanics to investigate sensitivity of midwall circumferential-radial shear strain Ecr to settings of parameters determining passive shear stiffness, cross-fiber active stress development, and transmural cross-over of myofibers. Simulated time courses of midwall LV Ecr were compared to time courses obtained in three healthy volunteers using MRT. Ecr as measured in the volunteers during the cardiac cycle was characterised by an amplitude of about 0.1. In the simulations, a realistic amplitude of the Ecr signal could be obtained by tuning either of the three model components mentioned above. However, a realistic time course of Ecr, with virtually no change of Ecr during isovolumic contraction and a correct base-to-apex g...</description>
            <author>Am J Physiol Heart C...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2598668</comments>
            <pubDate>Thu, 09 Jul 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2598668</guid>        </item>
        <item>
            <title>Focus on Carbon Monoxide: A Modulator of Neutrophil Oxidants and Elastase Spatial Localization?</title>
            <link>http://www.medworm.com/index.php?rid=2598667&amp;cid=s_29164_7_f&amp;fid=29164&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19592608%26dopt%3DAbstract</link>
            <description>Authors: Ganta VC, Alexander JS
    The protective roles of CO in various patho-physiological conditions are rapidly expanding. We are only beginning to understand how this gaseous signal molecule exerts such diverse cell and model specific effects. CO interacts in NO signaling, and is an activator of guanylate cyclase/PKG. However several downstream molecular signals mediated by CO (p38-MAPK, ERK1/2) may be oxidant dependent. How CO affects these and other signaling pathways in PMN is not well understood, but is of immense clinical interest. The present study by Mizoguchi et al. describes cell-specific roles of CORM-3 derived CO in protecting the lung against neutrophil dependent septic injury. Importantly, CO donors appear to only affect neutrophils and may involve a novel mechanism wher...</description>
            <author>Am J Physiol Heart C...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2598667</comments>
            <pubDate>Thu, 09 Jul 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2598667</guid>        </item>
        <item>
            <title>Reduction of Repolarization Reserve Unmasks the Pro-arrhythmic Role of Endogenous Late Sodium Current in the Heart.</title>
            <link>http://www.medworm.com/index.php?rid=2598666&amp;cid=s_29164_7_f&amp;fid=29164&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19592609%26dopt%3DAbstract</link>
            <description>Authors: Wu L, Rajamani S, Li H, January CT, Shryock JC, Belardinelli L
    Reduction of repolarization reserve increases the risk of arrhythmia. We hypothesized that inhibition of K(+) current (IK) to decrease repolarization reserve would unmask the pro-arrhythmic role of endogenous, physiological late Na(+) current (late INa). Monophasic action potentials (MAP) and 12-lead electrocardiogram were recorded from female rabbit isolated hearts. To block IK and reduce repolarization reserve, E-4031, 4-aminopyridine, and BaCl2 were used; to block endogenous late INa, tetrodotoxin (TTX) and ranolazine were used. E-4031 (1-60 nM) concentration-dependently prolonged MAP duration (MAPD90) and increased Tpeak-Tend, transmural dispersion (TDR), and beat-to-beat variability (BVR) of MAPD90. E-4031 cau...</description>
            <author>Am J Physiol Heart C...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2598666</comments>
            <pubDate>Thu, 09 Jul 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2598666</guid>        </item>
        <item>
            <title>Senescence, apoptosis, and stem cell biology: the rationale for an expanded view of intracrine action.</title>
            <link>http://www.medworm.com/index.php?rid=2598665&amp;cid=s_29164_7_f&amp;fid=29164&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19592610%26dopt%3DAbstract</link>
            <description>SENESCENCE, APOPTOSIS, AND STEM CELL BIOLOGY: THE RATIONALE FOR AN EXPANDED VIEW OF INTRACRINE ACTION.
    Am J Physiol Heart Circ Physiol. 2009 Jul 10;
    Authors: Re RN, Cook JL
    Some extracellular signaling peptides also at times function within the intracellular space. We have termed these peptides intracrines and have argued that intracrine function is associated with a wide variety of peptides/proteins including hormones, growth factors, cytokines, enzymes, and DNA binding proteins among others. Here we consider the possibility that intracrines participate in the related phenomena of senescence, apoptosis, and stem cell regulation of tissue biology. Based on this analysis, we also suggest that the concept of intracrine action be expanded to include possible regulatory peptide tra...</description>
            <author>Am J Physiol Heart C...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2598665</comments>
            <pubDate>Thu, 09 Jul 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2598665</guid>        </item>
        <item>
            <title>The absence of gp130 in dopamine {beta} hydroxylase-expressing neurons leads to autonomic imbalance and increased reperfusion arrhythmias.</title>
            <link>http://www.medworm.com/index.php?rid=2598664&amp;cid=s_29164_7_f&amp;fid=29164&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19592611%26dopt%3DAbstract</link>
            <description>Authors: Parrish DC, Alston EN, Rohrer H, Hermes SM, Aicher SA, Nkadi P, Woodward WR, Stubbusch J, Gardner RT, Habecker BA
    Inflammatory cytokines that act through gp130 are elevated in the heart after myocardial infarction and in heart failure. These cytokines are potent regulators of neurotransmitter and neuropeptide production in sympathetic neurons, but are also important for the survival of cardiac myocytes following damage to the heart. To examine the effect of gp130 cytokines on cardiac nerves we used gp130(DBH-Cre/lox) mice, which have a selective deletion of the gp130 cytokine receptor in neurons expressing dopamine beta hydroxylase (DBH). Basal sympathetic parameters including norepinephrine (NE) content, tyrosine hydroxylase expression, NE transporter expression, and sympathe...</description>
            <author>Am J Physiol Heart C...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2598664</comments>
            <pubDate>Thu, 09 Jul 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2598664</guid>        </item>
        <item>
            <title>Intermedin is a New Angiogenic Growth Factor.</title>
            <link>http://www.medworm.com/index.php?rid=2598663&amp;cid=s_29164_7_f&amp;fid=29164&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19592612%26dopt%3DAbstract</link>
            <description>In this study, we evaluated the role of IMD in angiogenesis in the ischemic hindlimb. Adenovirus containing human IMD or control adenovirus (Ad.Null) was injected into adductor muscles of rats immediately after femoral artery ligation. Expression of human IMD was detected in the skeletal muscle 5 days after viral injection. Blood perfusion in the ischemic hindlimb was monitored by laser Doppler imaging from 1 to 3 weeks after gene delivery. Compared to animals receiving Ad.Null, IMD gene transfer resulted in a time-dependent increase in blood perfusion. IMD gene delivery also increased capillary and arteriole density in ischemic hindlimb, identified by anti-CD-31 and alpha-smooth muscle actin immunostaining. Angiogenesis promoted by IMD was confirmed by increased capillary formation and he...</description>
            <author>Am J Physiol Heart C...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2598663</comments>
            <pubDate>Thu, 09 Jul 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2598663</guid>        </item>
        <item>
            <title>Myocardial lysyl oxidase regulation of cardiac remodeling in a murine model of diet-induced metabolic syndrome.</title>
            <link>http://www.medworm.com/index.php?rid=2598662&amp;cid=s_29164_7_f&amp;fid=29164&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19592613%26dopt%3DAbstract</link>
            <description>Authors: Zibadi S, Vazquez R, Moore D, Larson DF, Watson RR
    Metabolic syndrome (MetS) represents an increased risk of cardiovascular disease. Although its individual components adversely affect cardiac structure and function, the extent to which multiple components of MetS affect the cardiac extracellular matrix (ECM) has not been well characterized. Lysyl oxidase (LOX) is one of the cardiac ECM modifying enzymes that catalyzes the formation of collagen cross-linking. Our objective was to define the effect of diet-induced MetS on LOX enzyme. MetS was induced in male C57BL/6 mice by administrating a high-fat high-simple carbohydrate (HFHSC) diet for 6 months. Gene expression was determined by real-time PCR. The cardiac protein expression and enzymatic activity of LOX were measured. The ...</description>
            <author>Am J Physiol Heart C...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2598662</comments>
            <pubDate>Thu, 09 Jul 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2598662</guid>        </item>
        <item>
            <title>A1 adenosine receptor-mediated protein kinase C and p42/p44 mitogen-activated protein kinase signaling in mouse coronary artery smooth muscle cells.</title>
            <link>http://www.medworm.com/index.php?rid=2598661&amp;cid=s_29164_7_f&amp;fid=29164&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19592614%26dopt%3DAbstract</link>
            <description>This study was performed in coronary artery smooth muscle cells (CASMC) isolated from mouse heart (A1WT and A1KO) to delineate the A1AR signaling through protein kinase C (PKC) pathway. In A1WT cells, treatment with ENBA (10(-5)M) increased A1AR expression by 150%, which was inhibited significantly by A1AR antagonist, DPCPX (10(-6)M) but not in A1KO CASMC. PKC isoforms were identified by western blotting in cytosolic and membrane fractions from cell homogenates of CASMC. In A1WT and A1KO cells, significant levels of basal PKCalpha were detected in cytosolic fractions. Treatment with A1AR agonist, ENBA (10-5M) translocated PKCalpha from cytosolic to membrane fraction significantly in A1WT but not in A1KO. PLC isoforms (betaI, betaIII and gamma1) were analyzed using specific antibodies where...</description>
            <author>Am J Physiol Heart C...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2598661</comments>
            <pubDate>Thu, 09 Jul 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2598661</guid>        </item>
        <item>
            <title>The transport of LDL across the deformable arterial wall: the effect of endothelial cell turnover and intimal deformation under hypertension.</title>
            <link>http://www.medworm.com/index.php?rid=2598660&amp;cid=s_29164_7_f&amp;fid=29164&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19592615%26dopt%3DAbstract</link>
            <description>Authors: Dabagh Meshin M, Jalali P, Tarbell JM
    A multilayered model of the aortic wall is introduced to investigate the transport of low-density lipoprotein (LDL) under hypertension, taking into account the influences of increased endothelial cell turnover and deformation of the intima at higher pressure. Meanwhile, the thickness and properties of the endothelium, intima, internal elastic lamina (IEL), and media are affected by the transmural pressure. The LDL macromolecules enter the intima through leaky junctions over the endothelium, which are created by dying or dividing cells. Water molecules enter the intima via the paracellular pathway through breaks in tight junctions after passing the glycocalyx as well as through leaky junctions. The glycocalyx is modeled as a Brinkman porous...</description>
            <author>Am J Physiol Heart C...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2598660</comments>
            <pubDate>Thu, 09 Jul 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2598660</guid>        </item>
        <item>
            <title>Adipose-derived Stem Cells Are an Effective Cell Candidate for Treatment of Heart Failure - An MR Imaging Study of Rat Hearts.</title>
            <link>http://www.medworm.com/index.php?rid=2563682&amp;cid=s_29164_7_f&amp;fid=29164&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19574490%26dopt%3DAbstract</link>
            <description>This study was to assess the potential therapeutic efficacy of adipose-derived stem cells (ASCs) on infarcted hearts. Myocardial infarction was induced in rat hearts by occlusion of the left anterior descending (LAD) artery. One week after LAD occlusion, the rats were divided to three groups and subjected to transplantation of ASCs, transplantation of cell-culture medium (CCM) or remained untreated. During one-month recovery period, magnetic resonance (MR) imaging showed that the ASC-treated hearts had a significantly greater left ventricular ejection fraction (LVEF) and LV wall thickening than did the CCM-treated and untreated hearts. The capillary density in infarct border zone was significantly higher in the ASC-treated hearts than in the CCM-treated and untreated hearts. However, only ...</description>
            <author>Am J Physiol Heart C...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2563682</comments>
            <pubDate>Wed, 01 Jul 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2563682</guid>        </item>
        <item>
            <title>Hemoglobin vesicles improve wound healing and tissue survival in critically ischemic skin in mice.</title>
            <link>http://www.medworm.com/index.php?rid=2563681&amp;cid=s_29164_7_f&amp;fid=29164&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19574491%26dopt%3DAbstract</link>
            <description>Authors: Plock JA, Rafatmehr N, Sinovcic D, Schnider J, Sakai H, Tsuchida E, Banic A, Erni D
    Local hypoxia, as due to trauma, surgery or arterial occlusive disease, may severely jeopardize the survival of the affected tissue and its wound healing capacity. Initially developed to replace blood transfusions, artificial oxygen carriers have emerged as oxygen therapeutics in such conditions. The aim of this study was to target primary wound healing and survival in critically ischemic skin by systemic application of left-shifted liposomal hemoglobin vesicles (HbVs). This was tested in bilateral, cranially based dorsal skin flaps in mice treated with a HbV solution with an oxygen affinity that was increased to a P50 of 9 mmHg. Twenty percent of total blood volume of HbV solution were injecte...</description>
            <author>Am J Physiol Heart C...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2563681</comments>
            <pubDate>Wed, 01 Jul 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2563681</guid>        </item>
        <item>
            <title>Am J Physiol Heart Circ Physiol; +269 new citations</title>
            <link>http://www.medworm.com/index.php?rid=2531106&amp;cid=s_29164_7_f&amp;fid=29164&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fsites%2Fentrez%3Fcmd%3DSearch%26db%3Dpubmed%26term%3D%28%28%28Am%2520J%2520Physiol%2520Heart%2520Circ%2520Physiol%29%2520AND%2520%25222009%252F04%252F07%252007.02%2522%255BMHDA%255D%253A%25222009%252F06%252F27%252011.07%2522%255BMHDA%255D%29%29%2520NOT%2520%28%28%2520%28%28%28%2522Am%2520J%2520Physiol%2520Heart%2520Circ%2520Physiol%2522%255BTIAB%255D%29%29%29%2520AND%2520%25220001%2522%255BEDAT%255D%253A%25222009%252F04%252F07%252007.02%2522%255BEDAT%255D%29%29</link>
            <description>269 new pubmed citations were retrieved for your search.
Click on the search hyperlink below to display the complete search results:

Am J Physiol Heart Circ Physiol
These pubmed results were generated on 2009/06/27PubMed, a service of the National Library of Medicine, includes over 15 million 
citations for biomedical articles back to the 1950's.
These citations are from MEDLINE and additional life science journals. 
PubMed includes links to many sites providing full text articles and other related resources. (Source: Am J Physiol Heart C...)</description>
            <author>Am J Physiol Heart C...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2531106</comments>
            <pubDate>Sat, 27 Jun 2009 15:07:01 +0100</pubDate>
            <guid isPermaLink="false">2531106</guid>        </item>
        <item>
            <title>Patient-specific three-dimensional simulation of ldl accumulation in a human left coronary artery in its healthy and atherosclerotic states.</title>
            <link>http://www.medworm.com/index.php?rid=2306249&amp;cid=s_29164_7_f&amp;fid=29164&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19329764%26dopt%3DAbstract</link>
            <description>PATIENT-SPECIFIC THREE-DIMENSIONAL SIMULATION OF LDL ACCUMULATION IN A HUMAN LEFT CORONARY ARTERY IN ITS HEALTHY AND ATHEROSCLEROTIC STATES.
    Am J Physiol Heart Circ Physiol. 2009 Mar 27;
    Authors: Olgac U, Poulikakos D, Saur SC, Alkadhi H, Kurtcuoglu V
    We calculate low-density lipoprotein (LDL) transport from blood into arterial walls in a three-dimensional patient-specific model of a human left coronary artery. The in-vivo anatomy data are obtained from computed tomography (CT) images of a patient with coronary artery disease. Models of the artery anatomy in its healthy and diseased states are derived after segmentation of the vessel lumen with and without the detected plaque, respectively. Spatial shear stress distribution at the endothelium is determined through the reconstru...</description>
            <author>Am J Physiol Heart C...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2306249</comments>
            <pubDate>Fri, 27 Mar 2009 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">2306249</guid>        </item>
        <item>
            <title>Differences in Collagen Crosslinking Between the Four Valves of the Bovine Heart: A Possible Role in Adaptation to Mechanical Fatigue.</title>
            <link>http://www.medworm.com/index.php?rid=2306246&amp;cid=s_29164_7_f&amp;fid=29164&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19329765%26dopt%3DAbstract</link>
            <description>Authors: Aldous IG, Veres SP, Jahangir A, Lee JM
    Hydrothermal isometric tension (HIT) testing and high performance liquid chromatography (HPLC) were used to assess the molecular stability and crosslink population of collagen in the four valves of the adult bovine heart. Untreated and NaBH4-treated tissues under isometric tension were heated in a water bath to a 90 degrees C isotherm that was sustained for 5 hours. The denaturation temperature (Td), associated with hydrogen bond rupture and molecular stability, and the half-time of load decay (t1/2), associated with peptide bond hydrolysis and intermolecular crosslinking, were calculated from acquired load/temperature/time data. An unpaired group of samples of the same population was biochemically assayed for the types and quantities of...</description>
            <author>Am J Physiol Heart C...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2306246</comments>
            <pubDate>Fri, 27 Mar 2009 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">2306246</guid>        </item>
        <item>
            <title>Impact of Mitral Regurgitation on Left Ventricular Anatomic and Molecular Remodeling and Systolic Function: Implication for Outcome.</title>
            <link>http://www.medworm.com/index.php?rid=2306243&amp;cid=s_29164_7_f&amp;fid=29164&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19329766%26dopt%3DAbstract</link>
            <description>Conclusion: Chronic MR leads to LV anatomic and cellular remodeling and impaired contractility. The time course of LV remodeling and function changes in the rat model of MR is similar to humans. Prediction of outcome may be achieved by assessments of early LV remodeling. Key words: mitral regurgitation, Molecular biology, left ventricular remodeling, left ventricular function.
    PMID: 19329766 [PubMed - as supplied by publisher] (Source: Am J Physiol Heart C...)</description>
            <author>Am J Physiol Heart C...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2306243</comments>
            <pubDate>Fri, 27 Mar 2009 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">2306243</guid>        </item>
        <item>
            <title>Venomotion Modulates Lymphatic Pumping in the Bat Wing.</title>
            <link>http://www.medworm.com/index.php?rid=2306240&amp;cid=s_29164_7_f&amp;fid=29164&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19329767%26dopt%3DAbstract</link>
            <description>Authors: Dongaonkar RM, Stewart RH, Laine GA, Davis MJ, Zawieja DC, Quick CM
    In skin, it is believed that lymph must be pumped by intrinsic contraction of lymphatic muscle, since investigators have not considered that cyclical dilation of adjacent venules could compress adjacent lymphatic microvessels. Because lymphatic vessels are sensitive to stretch, we hypothesized that venomotion not only can cause extrinsic pumping of lymph in nearby lymphatic vessels, but also can stimulate intrinsic contractions. Bat wing venules have pronounced venomotion and are in close proximity to lymphatic microvessels, and can be studied noninvasively without the confounding effects of anesthesia, surgical trauma, or contrast agents. Therefore, the interaction between venules and their paired lymphatic v...</description>
            <author>Am J Physiol Heart C...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2306240</comments>
            <pubDate>Fri, 27 Mar 2009 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">2306240</guid>        </item>
        <item>
            <title>Myocardial oxygenation is critical for improving regeneration capacity.</title>
            <link>http://www.medworm.com/index.php?rid=2306237&amp;cid=s_29164_7_f&amp;fid=29164&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19329768%26dopt%3DAbstract</link>
            <description>Authors: Kaushal S, Bouchard CP, Wold LE
    No abstract Key words: stem cell, myocardial infarction, ejection fraction, cellular cardiomyoplasty.
    PMID: 19329768 [PubMed - as supplied by publisher] (Source: Am J Physiol Heart C...)</description>
            <author>Am J Physiol Heart C...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2306237</comments>
            <pubDate>Fri, 27 Mar 2009 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">2306237</guid>        </item>
        <item>
            <title>Distributed modeling of osmotically driven fluid transport in peritoneal dialysis: theoretical and computational investigations.</title>
            <link>http://www.medworm.com/index.php?rid=2306234&amp;cid=s_29164_7_f&amp;fid=29164&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19329769%26dopt%3DAbstract</link>
            <description>Authors: Waniewski J, Stachowska-Pietka J, Flessner M
    Based on a distributed model of peritoneal transport, a mathematical theory is presented to explain how the osmotic agent in the peritoneal dialysis solution that penetrates tissue induces osmotically driven flux out of the tissue. The relationships between phenomenological transport parameters (hydraulic permeability, reflection coefficient) and the respective specific transport parameters for the tissue and the capillary wall are separately described. Closed formulas for steady state flux across the peritoneal surface and for hydrostatic pressure at the opposite surface are obtained using an approximate description of the concentration profile of the osmotic agent within the tissue by exponential function. A case of experimental s...</description>
            <author>Am J Physiol Heart C...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2306234</comments>
            <pubDate>Fri, 27 Mar 2009 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">2306234</guid>        </item>
        <item>
            <title>Dose-response relationship of autonomic nervous system responses to individualized training impulse in marathon runners.</title>
            <link>http://www.medworm.com/index.php?rid=2306232&amp;cid=s_29164_7_f&amp;fid=29164&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19329770%26dopt%3DAbstract</link>
            <description>DOSE-RESPONSE RELATIONSHIP OF AUTONOMIC NERVOUS SYSTEM RESPONSES TO INDIVIDUALIZED TRAINING IMPULSE IN MARATHON RUNNERS.
    Am J Physiol Heart Circ Physiol. 2009 Mar 27;
    Authors: Manzi V, Castagna C, Padua E, Lombardo M, D'Ottavio S, Massaro MC, Volterrani M, Iellamo F
    In athletes exercise training induces autonomic nervous system (ANS) adaptations that could be used to monitor the training status. However, the relationship between training and ANS in athletes has been investigated without regard for individual training loads. We tested the hypothesis that in long-distance athletes changes in ANS parameters are dose-response related to individual volume/intensity training load (TL) and could predict athletic performance. Spectral analysis of HR and systolic arterial pressure (SAP)...</description>
            <author>Am J Physiol Heart C...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2306232</comments>
            <pubDate>Fri, 27 Mar 2009 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">2306232</guid>        </item>
        <item>
            <title>Am J Physiol Heart Circ Physiol; +28 new citations</title>
            <link>http://www.medworm.com/index.php?rid=2276447&amp;cid=s_29164_7_f&amp;fid=29164&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Fcmd%3DSearch%26db%3DPubMed%26term%3D%2528%2528%2528Am%2BJ%2BPhysiol%2BHeart%2BCirc%2BPhysiol%2529%2BAND%2B%25222009%252F03%252F14%2B18%252E35%2522%255BMHDA%255D%253A%25222009%252F03%252F20%2B07%252E08%2522%255BMHDA%255D%2529%2529%2BNOT%2B%2528%2528%2B%2528%2528Am%2BJ%2BPhysiol%2BHeart%2BCirc%2BPhysiol%255BTIAB%255D%2529%2529%2BAND%2B%25220001%2522%255BEDAT%255D%253A%25222009%252F03%252F14%2B18%252E35%2522%255BEDAT%255D%2529%2529</link>
            <description>28 new PubMed citations were retrieved for your search.
Click on the search hyperlink below to display the complete search results:

Am J Physiol Heart Circ Physiol
These PubMed results were generated on 2009/03/20PubMed, a service of the National Library of Medicine, includes over 15 million 
citations for biomedical articles back to the 1950's.
These citations are from MEDLINE and additional life science journals. 
PubMed includes links to many sites providing full text articles and other related resources. (Source: Am J Physiol Heart C...)</description>
            <author>Am J Physiol Heart C...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2276447</comments>
            <pubDate>Fri, 20 Mar 2009 11:08:29 +0100</pubDate>
            <guid isPermaLink="false">2276447</guid>        </item>
        <item>
            <title>Am J Physiol Heart Circ Physiol; +63 new citations</title>
            <link>http://www.medworm.com/index.php?rid=2269813&amp;cid=s_29164_7_f&amp;fid=29164&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Fcmd%3DSearch%26db%3DPubMed%26term%3D%2528%2528%2528Am%2BJ%2BPhysiol%2BHeart%2BCirc%2BPhysiol%2529%2BAND%2B%25222009%252F03%252F11%2B06%252E54%2522%255BMHDA%255D%253A%25222009%252F03%252F14%2B18%252E34%2522%255BMHDA%255D%2529%2529%2BNOT%2B%2528%2528%2B%2528%2528Am%2BJ%2BPhysiol%2BHeart%2BCirc%2BPhysiol%255BTIAB%255D%2529%2529%2BAND%2B%25220001%2522%255BEDAT%255D%253A%25222009%252F03%252F11%2B06%252E54%2522%255BEDAT%255D%2529%2529%26itool%3Drss</link>
            <description>63 new PubMed citations were retrieved for your search.
Click on the search hyperlink below to display the complete search results:

Am J Physiol Heart Circ Physiol
These PubMed results were generated on 2009/03/14PubMed, a service of the National Library of Medicine, includes over 15 million 
citations for biomedical articles back to the 1950's.
These citations are from MEDLINE and additional life science journals. 
PubMed includes links to many sites providing full text articles and other related resources. (Source: Am J Physiol Heart C...)</description>
            <author>Am J Physiol Heart C...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2269813</comments>
            <pubDate>Sat, 14 Mar 2009 22:34:17 +0100</pubDate>
            <guid isPermaLink="false">2269813</guid>        </item>
        <item>
            <title>Am J Physiol Heart Circ Physiol; +63 new citations</title>
            <link>http://www.medworm.com/index.php?rid=2262921&amp;cid=s_29164_7_f&amp;fid=29164&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Fcmd%3DSearch%26db%3DPubMed%26term%3D%2528%2528%2528Am%2BJ%2BPhysiol%2BHeart%2BCirc%2BPhysiol%2529%2BAND%2B%25222009%252F03%252F11%2B06%252E54%2522%255BMHDA%255D%253A%25222009%252F03%252F14%2B18%252E34%2522%255BMHDA%255D%2529%2529%2BNOT%2B%2528%2528%2B%2528%2528Am%2BJ%2BPhysiol%2BHeart%2BCirc%2BPhysiol%255BTIAB%255D%2529%2529%2BAND%2B%25220001%2522%255BEDAT%255D%253A%25222009%252F03%252F11%2B06%252E54%2522%255BEDAT%255D%2529%2529</link>
            <description>63 new PubMed citations were retrieved for your search.
Click on the search hyperlink below to display the complete search results:

Am J Physiol Heart Circ Physiol
These PubMed results were generated on 2009/03/14PubMed, a service of the National Library of Medicine, includes over 15 million 
citations for biomedical articles back to the 1950's.
These citations are from MEDLINE and additional life science journals. 
PubMed includes links to many sites providing full text articles and other related resources. (Source: Am J Physiol Heart C...)</description>
            <author>Am J Physiol Heart C...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2262921</comments>
            <pubDate>Sat, 14 Mar 2009 22:34:17 +0100</pubDate>
            <guid isPermaLink="false">2262921</guid>        </item>
        <item>
            <title>Sex Differences and Central Protective Effect of 17{beta}-estradiol in the Development of Aldosterone/NaCl-induced Hypertension.</title>
            <link>http://www.medworm.com/index.php?rid=2251249&amp;cid=s_29164_7_f&amp;fid=29164&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19270192%26dopt%3DAbstract</link>
            <description>Authors: Xue B, Badaue-Passos D, Guo F, Gomez-Sanchez CE, Hay M, Johnson AK
    The present study tested the hypotheses that male and female rats respond differently to subcutaneous infusions of aldosterone (ALDO; 1.8 microg/kg/h, 1% NaCl to drink, 28 days) and that central estrogen plays a protective role against the development of hypertension. In rats with blood pressure (BP) and heart rate (HR) measured by DSI(R) telemetry, chronic ALDO/NaCl treatment induced a greater increase in BP in males (Delta25.4+/-2.4 mmHg) than in females (Delta7.1+/-2.2 mmHg). Gonadectomy augmented ALDO/NaCl-induced hypertension in females (Delta18.2+/-2.0 mmHg) but had no effect in males (Delta23.1+/-2.9 mmHg). Immunohistochemistry for Fra-like activity was higher in the paraventricular nucleus of intact mal...</description>
            <author>Am J Physiol Heart C...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2251249</comments>
            <pubDate>Fri, 06 Mar 2009 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">2251249</guid>        </item>
        <item>
            <title>Glutathione S-transferase P protects against endothelial dysfunction induced by exposure to tobacco smoke.</title>
            <link>http://www.medworm.com/index.php?rid=2251248&amp;cid=s_29164_7_f&amp;fid=29164&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19270193%26dopt%3DAbstract</link>
            <description>Authors: Conklin DJ, Haberzettl P, Prough RA, Bhatnagar A
    Exposure to tobacco smoke impairs endothelium-dependent arterial dilation. Reactive constituents of cigarette smoke are metabolized and detoxified by glutathione S-transferases (GSTs). Although polymorphisms in GST genes are associated with the risk of cancer in smokers, the role of these enzymes in regulating the cardiovascular effects of smoking has not been studied. The P isoform of GST, which catalyzes the conjugation of electrophilic molecules in cigarette smoke such as acrolein, was expressed in high abundance in mouse lung and aorta. Exposure to tobacco smoke for 3 days (5h/day) decreased total plasma protein. These changes were exaggerated in GSTP(-/-) mice. Aortic rings isolated from tobacco smoke-exposed GSTP(-/-) mice...</description>
            <author>Am J Physiol Heart C...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2251248</comments>
            <pubDate>Fri, 06 Mar 2009 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">2251248</guid>        </item>
        <item>
            <title>Am J Physiol Heart Circ Physiol; +18 new citations</title>
            <link>http://www.medworm.com/index.php?rid=2229971&amp;cid=s_29164_7_f&amp;fid=29164&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Fcmd%3DSearch%26db%3DPubMed%26term%3D%2528%2528%2528Am%2BJ%2BPhysiol%2BHeart%2BCirc%2BPhysiol%2529%2BAND%2B%25222009%252F02%252F26%2B05%252E07%2522%255BMHDA%255D%253A%25222009%252F03%252F04%2B06%252E30%2522%255BMHDA%255D%2529%2529%2BNOT%2B%2528%2528%2B%2528%2528Am%2BJ%2BPhysiol%2BHeart%2BCirc%2BPhysiol%255BTIAB%255D%2529%2529%2BAND%2B%25220001%2522%255BEDAT%255D%253A%25222009%252F02%252F26%2B05%252E07%2522%255BEDAT%255D%2529%2529</link>
            <description>18 new PubMed citations were retrieved for your search.
Click on the search hyperlink below to display the complete search results:

Am J Physiol Heart Circ Physiol
These PubMed results were generated on 2009/03/04PubMed, a service of the National Library of Medicine, includes over 15 million 
citations for biomedical articles back to the 1950's.
These citations are from MEDLINE and additional life science journals. 
PubMed includes links to many sites providing full text articles and other related resources. (Source: Am J Physiol Heart C...)</description>
            <author>Am J Physiol Heart C...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2229971</comments>
            <pubDate>Wed, 04 Mar 2009 11:26:24 +0100</pubDate>
            <guid isPermaLink="false">2229971</guid>        </item>
        <item>
            <title>Pka phosphorylation of herg protein regulates the rate of channel synthesis.</title>
            <link>http://www.medworm.com/index.php?rid=2214298&amp;cid=s_29164_7_f&amp;fid=29164&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19234087%26dopt%3DAbstract</link>
            <description>We examined the effects of prolonged PKA activity on the HERG K(+) channel in stably transfected HEK cells. Sustained elevation of cAMP by either CPT-cAMP or forskolin increased the HERG channel protein abundance 2-4-fold within 24 hours, with measurable difference as early as four hours. The cAMP-induced augmentation was not due to changes in transcription and was specific for HERG compared to other cardiac K(+) channels (Kv1.4, Kv1.5, Kir2.1 and KvLQT1). PKA activity was necessary for the effect on HERG protein and did not involve other cAMP signaling pathways. Direct PKA phosphorylation of the HERG protein was responsible for the cAMP-induced augmentation. Enhanced abundance of HERG protein was detected in ER, Golgi and plasma membrane without significant changes in trafficking rates or...</description>
            <author>Am J Physiol Heart C...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2214298</comments>
            <pubDate>Fri, 20 Feb 2009 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">2214298</guid>        </item>
        <item>
            <title>Both central command and exercise pressor reflex activate cardiac sympathetic nerve activity in decerebrate cats.</title>
            <link>http://www.medworm.com/index.php?rid=2214297&amp;cid=s_29164_7_f&amp;fid=29164&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19234088%26dopt%3DAbstract</link>
            <description>Authors: Tsuchimochi H, Hayes SG, McCord JL, Kaufman MP
    Both static and dynamic exercise are known to increase cardiac pump function as well as arterial blood pressure. Feedforward control by central command and feedback control by the exercise pressor reflex are thought to be the neural mechanisms causing these effects during exercise. To date, it remains unknown how each mechanism activates cardiac sympathetic nerve activity (CSNA) during exercise, especially at its onset. Thus, we examined the response of CSNA to stimulation of the mesencephalic locomotor region (MLR, i.e., central command) and to static muscle contraction of the triceps surae muscles or stretch of the calcaneal tendon in decerebrate cats. We found that MLR stimulation immediately increased CSNA, which was followed ...</description>
            <author>Am J Physiol Heart C...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2214297</comments>
            <pubDate>Fri, 20 Feb 2009 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">2214297</guid>        </item>
        <item>
            <title>Sphingolipid signaling and treatment during remodeling of the uninfarcted ventricular wall after myocardial infarction.</title>
            <link>http://www.medworm.com/index.php?rid=2214296&amp;cid=s_29164_7_f&amp;fid=29164&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19234089%26dopt%3DAbstract</link>
            <description>Conclusion: These results provide the first documentation of alterations in S1P-mediated signaling during the in situ development of cardiomyopathy, and suggest a possible therapeutic role for pharmacologic S1P receptor agonism in the post-MI heart. Key words: Sphingosine 1-phosphate, Remodeling, Myocardial infarction, Apoptosis.
    PMID: 19234089 [PubMed - as supplied by publisher] (Source: Am J Physiol Heart C...)</description>
            <author>Am J Physiol Heart C...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2214296</comments>
            <pubDate>Fri, 20 Feb 2009 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">2214296</guid>        </item>
        <item>
            <title>IL-6 Loss Causes Ventricular Dysfunction, Fibrosis, Reduced Capillary Density and Dramatically Alters the Cell Populations of the Developing and Adult Heart.</title>
            <link>http://www.medworm.com/index.php?rid=2214295&amp;cid=s_29164_7_f&amp;fid=29164&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19234091%26dopt%3DAbstract</link>
            <description>In this study, we examine the effects of IL-6-deficiency on the cardiac cell populations, cardiac function and interactions between the cells of the heart, specifically cardiac fibroblasts and myocytes. To examine the effects of IL-6-loss on cardiac function, we used the IL-6(-/-) mouse. IL-6-deficiency caused severe cardiac dilatation, increased accumulation of interstitial collagen and altered expression of the adhesion protein periostin. In addition, flow cytometric analyses demonstrated dramatic alterations in the cardiac cell populations of IL-6(-/- )mice when compared to wild type littermates. We observed a marked increase in the cardiac fibroblast population in IL-6(-/-) mice, while a concommitment decrease was observed in the other cardiac cell populations examined. Moreover, we ob...</description>
            <author>Am J Physiol Heart C...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2214295</comments>
            <pubDate>Fri, 20 Feb 2009 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">2214295</guid>        </item>
        <item>
            <title>Activation of Caspase-3 may not Contribute to Post-Resuscitation Myocardial Dysfunction.</title>
            <link>http://www.medworm.com/index.php?rid=2214294&amp;cid=s_29164_7_f&amp;fid=29164&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19234092%26dopt%3DAbstract</link>
            <description>Authors: Radhakrishnan J, Ayoub IM, Gazmuri RJ
    We have previously reported that post-resuscitation myocardial dysfunction is accompanied by release of cytochrome c and caspase-3 activation. We now investigated the role of caspase-3 activation by examining whether such process prompts apoptotic DNA fragmentation, whether caspase-3 inhibition attenuates myocardial dysfunction, and whether myocardial protective effects of sodium-hydrogen exchanger isoform-1 (NHE-1) inhibition involve caspase-3 inhibition using a rat model of ventricular fibrillation (VF) of closed-chest resuscitation. Resuscitation after 4 or 8 minutes of untreated VF caused significant reductions in left ventricular stroke work index averaging 23% of sham control rats at 4 hours post-resuscitation. Left ventricular dysfu...</description>
            <author>Am J Physiol Heart C...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2214294</comments>
            <pubDate>Fri, 20 Feb 2009 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">2214294</guid>        </item>
        <item>
            <title>Endothelial heparanase secretion after acute hypoinsulinemia is regulated by glucose and fatty acid.</title>
            <link>http://www.medworm.com/index.php?rid=2193376&amp;cid=s_29164_7_f&amp;fid=29164&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19218500%26dopt%3DAbstract</link>
            <description>We examined how hyperglycemia controls secretion of heparanase, the enzyme that cleaves myocyte HSPG to initiate this movement. Diazoxide (DZ) was used to decrease serum insulin and generate hyperglycemia. A modified Langendorff technique was used to separate coronary from interstitial effluent, which were assayed for heparanase and LPL. Within 30 min of DZ, interstitial heparanase increased, an effect that closely mirrored an augmentation in interstitial LPL. Endothelial cells were incubated with palmitic acid (PA) or glucose, and heparanase secretion determined. PA increased intracellular heparanase, with no effect on secretion of this enzyme. Unlike PA, glucose dose-dependently lowered endothelial intracellular heparanase, which was strongly associated with increased heparanase activity...</description>
            <author>Am J Physiol Heart C...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2193376</comments>
            <pubDate>Fri, 13 Feb 2009 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">2193376</guid>        </item>
        <item>
            <title>Advanced Methods for Quantification of Infarct Size in Mice Using Three-Dimensional High-Field Late Gadolinium Enhancement MRI.</title>
            <link>http://www.medworm.com/index.php?rid=2193375&amp;cid=s_29164_7_f&amp;fid=29164&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19218501%26dopt%3DAbstract</link>
            <description>Authors: Bohl S, Lygate CA, Barnes H, Medway DJ, Stork LA, Schulz-Menger J, Neubauer S, Schneider JE
    Conventional methods to quantify infarct size after myocardial infarction in mice are not ideal, requiring either tissue destruction for histology, or relying on non-direct measurements such as wall motion. We therefore implemented a fast, high-resolution method to directly measure infarct size in vivo using three-dimensional Late-Gadolinium-Enhancement MRI (3D-LGE). Myocardial T1-relaxation was quantified at 9.4 Tesla in 5 mice, and reproducibility tested by repeat imaging after five days. In a separate set of healthy and infarcted mice (n=6 of each), continuous T1-measurements were made following intravenous (IV) or intraperitoneal (IP) injection of contrast agent (0.5micromol/g Gadol...</description>
            <author>Am J Physiol Heart C...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2193375</comments>
            <pubDate>Fri, 13 Feb 2009 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">2193375</guid>        </item>
        <item>
            <title>Rho-Kinase-Mediated Suppression of KDR Current in Cerebral Arteries Requires an Intact Actin Cytoskeleton.</title>
            <link>http://www.medworm.com/index.php?rid=2193374&amp;cid=s_29164_7_f&amp;fid=29164&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19218502%26dopt%3DAbstract</link>
            <description>This study examined the role of the actin cytoskeleton in Rho-kinase-mediated suppression of the delayed rectifier K(+) (KDR) current in cerebral arteries. Myocytes from rat cerebral arteries were enzymatically isolated and whole cell KDR currents monitored using conventional patch clamp electrophysiology. At +40 mV, the KDR current averaged 19.8 +/- 1.6 pA/pF (mean +/- SE) and was potently inhibited by uridine triphosphate (UTP; 3 x 10(-5) M). This suppression was observed to depend on Rho-signaling and was abolished by the Rho-kinase inhibitors H-1152 (3 x 10(-7) M) and Y-27632 (3 x 10(-5) M). Rho-kinase was also found to concomitantly facilitate actin polymerization in response to UTP. We therefore examined whether actin dynamics played a role in the ability of Rho-kinase to suppress KD...</description>
            <author>Am J Physiol Heart C...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2193374</comments>
            <pubDate>Fri, 13 Feb 2009 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">2193374</guid>        </item>
        <item>
            <title>Differential regulation of angiotensin-(1-12) in plasma and cardiac tissue in response to bilateral nephrectomy.</title>
            <link>http://www.medworm.com/index.php?rid=2193373&amp;cid=s_29164_7_f&amp;fid=29164&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19218503%26dopt%3DAbstract</link>
            <description>We examined the effects of 48 h bilateral nephrectomy on plasma and cardiac tissue expression of angiotensin (Ang)-(1-12) [Ang-(1-12)], Ang I, and Ang II of adult WKY to evaluate functional changes induced by removal of renal renin. The goal was to uncover additional evidence for an alternate role of Ang-(1-12) in forming Ang peptides independent of renal renin. The anephric state caused divergent effects on circulating and cardiac Ang-(1-12), Ang I, and Ang II content since the plasma levels of the peptides decreased, but increased markedly in the heart of nephrectomized WKY rats compared to sham-operated controls. A 34% decrease in plasma Ang-(1-12) levels post-nephrectomy was associated with a 78% and 66% decrease in plasma Ang I and Ang II, respectively (p &amp;lt; 0.05 versus sham). In co...</description>
            <author>Am J Physiol Heart C...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2193373</comments>
            <pubDate>Fri, 13 Feb 2009 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">2193373</guid>        </item>
        <item>
            <title>Cardiac systolic and diastolic function during whole-body heat stress.</title>
            <link>http://www.medworm.com/index.php?rid=2193372&amp;cid=s_29164_7_f&amp;fid=29164&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19218504%26dopt%3DAbstract</link>
            <description>Authors: Brothers RM, Bhella PS, Shibata S, Wingo JE, Levine BD, Crandall CG
    During a whole-body heat stress, stroke volume is either maintained or slightly elevated despite reduced ventricular filling pressures and central blood volume, suggestive of improved cardiac diastolic and / or systolic function. Heat stress improves cardiac systolic and diastolic function in patients with congestive heart failure, although it remains unknown whether similar responses occur in healthy individuals, which is the hypothesis to be tested. Nine male volunteers underwent a whole-body heat stress. Echocardiographic indices of diastolic and systolic function were performed following a supine resting period, and again following an increase in internal temperature of ~ 1.0 degrees C via passive heat str...</description>
            <author>Am J Physiol Heart C...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2193372</comments>
            <pubDate>Fri, 13 Feb 2009 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">2193372</guid>        </item>
        <item>
            <title>Translocon closure to Ca2+ leak in proliferating vascular smooth muscle cells.</title>
            <link>http://www.medworm.com/index.php?rid=2193371&amp;cid=s_29164_7_f&amp;fid=29164&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19218505%26dopt%3DAbstract</link>
            <description>Authors: Amer MS, Li J, O'Regan DJ, Steele DS, Porter KE, Sivaprasadarao A, Beech DJ
    Vascular smooth muscle cells have a proliferative phenotype that is important in vascular development, adaptation and disease. Intracellular calcium-handling is thought to play pivotal roles in determining the properties of these cells and thus previously unrecognized mechanisms for transmembrane calcium movement are of potential interest. An unsolved question is the mechanism of constitutive (passive) calcium leak from the intracellular stores. Studies of other cell types have suggested the translocon is a calcium leak pathway. Here we investigated the translocon's contribution in proliferating vascular smooth muscle cells. Calcium leak into the cytoplasm was measured using fura-2 and protein synthesi...</description>
            <author>Am J Physiol Heart C...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2193371</comments>
            <pubDate>Fri, 13 Feb 2009 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">2193371</guid>        </item>
        <item>
            <title>Physiological roles of A1 and A2A adenosine receptors in regulating heart rate, temperature and locomotion as revealed using knock-out mice and caffeine.</title>
            <link>http://www.medworm.com/index.php?rid=2193370&amp;cid=s_29164_7_f&amp;fid=29164&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19218506%26dopt%3DAbstract</link>
            <description>Authors: Yang JN, Chen JF, Fredholm BB
    Heart rate (HR), body temperature (TEMP), locomotor activity (LA) and oxygen consumption (O2C) were studied in awake mice lacking one or both of the adenosine A1 or A2A receptors (AR) using telemetry and respirometry, before and after caffeine administration. All parameters were lower during day than night and higher in females than males. Compared to wild-type (WT) littermates, HR was higher in male A1R knockout (KO) mice but lower in A2ARKO mice and intermediate in A1-A2AR double KO. A single dose of an unselective beta-blocker (timolol, 1 mg/kg) abolished the HR differences between these genotypes. Deletion of A1Rs had little effect on TEMP, whereas deletion of A2ARs increased it in females and decreased it in males. A1-A2ARKO mice had lower TE...</description>
            <author>Am J Physiol Heart C...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2193370</comments>
            <pubDate>Fri, 13 Feb 2009 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">2193370</guid>        </item>
        <item>
            <title>Role of ROCK1/2 in vascular branching.</title>
            <link>http://www.medworm.com/index.php?rid=2193369&amp;cid=s_29164_7_f&amp;fid=29164&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19218507%26dopt%3DAbstract</link>
            <description>Authors: van Nieuw Amerongen GP, van Hinsbergh VW
    No Abstract Key words: Angiogenesis, rho kinase, endothelium.
    PMID: 19218507 [PubMed - as supplied by publisher] (Source: Am J Physiol Heart C...)</description>
            <author>Am J Physiol Heart C...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2193369</comments>
            <pubDate>Fri, 13 Feb 2009 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">2193369</guid>        </item>
        <item>
            <title>Reversal of Cardiac Myocyte Dysfunction as a Unique Mechanism of Rescue by P2X4 Receptors in Cardiomyopathy.</title>
            <link>http://www.medworm.com/index.php?rid=2176456&amp;cid=s_29164_7_f&amp;fid=29164&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19201994%26dopt%3DAbstract</link>
            <description>Authors: Shen JB, Shutt RH, Agosto M, Pappano AJ, Liang BT
    Binary cardiac transgenic (Tg) overexpression of P2X4 receptors (P2X4R) improved survival of the cardiomyopathic calsequestrin (CSQ) mice. Here we studied the mechanism of rescue using binary P2X4R/CSQ Tg and CSQ Tg mice as models. Cellular and intact heart properties were determined by simultaneous sarcomere shortening and Ca(2+) transients in vitro and echocardiography in vivo. Similar to a delay in death, binary mice exhibited a slowed heart failure progression with a greater LV fractional shortening (FS) and thickness and a concomitant lesser degree of LV dilatation in both systole and diastole at 8 or 12 weeks. By 16 weeks, binary hearts showed similarly depressed FS and thinned out LV, and equal enlargement of LV as did 1...</description>
            <author>Am J Physiol Heart C...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2176456</comments>
            <pubDate>Fri, 06 Feb 2009 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">2176456</guid>        </item>
        <item>
            <title>Mechanical work and energetic analysis of eccentric cardiac remodeling in a volume overload heart failure in rats.</title>
            <link>http://www.medworm.com/index.php?rid=2176455&amp;cid=s_29164_7_f&amp;fid=29164&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19201995%26dopt%3DAbstract</link>
            <description>In conclusion, volume-overloaded failing rat hearts were characterized by marked contractile dysfunction accompanied by a less efficient energy utilization in Ca(2+) handling processes. Present results suggest the possibility that repairing Ca(2+) handling in excitation-contraction coupling would improve the contractility of the myocardium after eccentric cardiac remodeling. Key words: heart failure, cardiomyopathy, volume overload, rat.
    PMID: 19201995 [PubMed - as supplied by publisher] (Source: Am J Physiol Heart C...)</description>
            <author>Am J Physiol Heart C...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2176455</comments>
            <pubDate>Fri, 06 Feb 2009 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">2176455</guid>        </item>
        <item>
            <title>Greater fractalkine expression in mesenteric arteries of female spontaneously hypertensive rats compared to males.</title>
            <link>http://www.medworm.com/index.php?rid=2176454&amp;cid=s_29164_7_f&amp;fid=29164&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19201996%26dopt%3DAbstract</link>
            <description>In conclusion, urinary and vascular markers of inflammation are greater in female SHR compared to males, although blood pressure and cardiovascular risk are less in females. Key words: hypertension, inflammation, gener, microarray.
    PMID: 19201996 [PubMed - as supplied by publisher] (Source: Am J Physiol Heart C...)</description>
            <author>Am J Physiol Heart C...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2176454</comments>
            <pubDate>Fri, 06 Feb 2009 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">2176454</guid>        </item>
        <item>
            <title>Calcium influx-dependent differential actions of superoxide and hydrogen peroxide on microvessel permeability.</title>
            <link>http://www.medworm.com/index.php?rid=2176453&amp;cid=s_29164_7_f&amp;fid=29164&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19201997%26dopt%3DAbstract</link>
            <description>This study aims to define the individual roles of hydrogen peroxide, H2O2, and superoxide in ROS-induced increases in permeability and endothelial [Ca(2+)]i in individually perfused rat mesenteric venules. Microvessel permeability was determined by measuring hydraulic conductivity (Lp). Endothelial [Ca(2+)]i was measured in fura-2-AM-loaded microvessels. Perfusing microvessels with superoxide generated by hypoxanthine and xanthine oxidase, HX/XO, induced immediate and transient increases in microvessel Lp. The mean peak value, occurred within 5 min of HX/XO exposure, was 4.3 +/- 0.6 times that of the control. In contrast, perfusion of H2O2 (100 and 500 microM) caused no immediate increases in Lp. A significant Lp increase, 3.6 +/- 0.6 times the control value, occurred 30 min after perfusio...</description>
            <author>Am J Physiol Heart C...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2176453</comments>
            <pubDate>Fri, 06 Feb 2009 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">2176453</guid>        </item>
        <item>
            <title>Slowing of Cardiomyocyte Ca2+ Release and Contraction During Heart Failure Progression in Post-Infarction Mice.</title>
            <link>http://www.medworm.com/index.php?rid=2176452&amp;cid=s_29164_7_f&amp;fid=29164&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19201998%26dopt%3DAbstract</link>
            <description>We examined the progression of in vivo and in vitro alterations in contractile function in CHF mice, and investigated underlying alterations in Ca(2+) homeostasis. Following induction of myocardial infarction (MI), mice with CHF were examined at early (1-week post-MI) and chronic (10-weeks post-MI) stages of disease development. SHAM-operated mice served as controls. Global and local left ventricle function were assessed by echocardiography in sedated animals (~2% isoflurane). Excitation-contraction coupling was examined in cardiomyocytes isolated from the viable septum. CHF progression between 1-week and 10-weeks post-MI resulted in increased mortality, development of hypertrophy, and deterioration of global left ventricular function. Local function in the non-infarcted myocardium also de...</description>
            <author>Am J Physiol Heart C...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2176452</comments>
            <pubDate>Fri, 06 Feb 2009 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">2176452</guid>        </item>
        <item>
            <title>Inhibition of p38 MAP Kinase Reverses Hypoxia Induced Pulmonary Artery Endothelial Dysfunction.</title>
            <link>http://www.medworm.com/index.php?rid=2176451&amp;cid=s_29164_7_f&amp;fid=29164&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19201999%26dopt%3DAbstract</link>
            <description>Conclusion: Pharmacological inhibition of p38 MAP kinase was effective in increasing NO generation, reducing superoxide burden and restoring hypoxia induced endothelial dysfunction in rats with hypoxia-induced pulmonary hypertension. p38 MAP kinase may be a novel target for treatment of pulmonary hypertension. Key words: Pulmonary Hypertension, Hypoxia, p38 MAP kinase, Endothelium.
    PMID: 19201999 [PubMed - as supplied by publisher] (Source: Am J Physiol Heart C...)</description>
            <author>Am J Physiol Heart C...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2176451</comments>
            <pubDate>Fri, 06 Feb 2009 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">2176451</guid>        </item>
        <item>
            <title>Differential involvement of COX1 and COX2 in the vasculopathy associated with the {alpha}-galactosidase-A knockout mouse.</title>
            <link>http://www.medworm.com/index.php?rid=2176450&amp;cid=s_29164_7_f&amp;fid=29164&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19202000%26dopt%3DAbstract</link>
            <description>Authors: Park JL, Shu L, Shayman JA
    The lysosomal storage disorder, Fabry disease, is characterized by excessive globotriaosylceramide (Gb3) accumulation in major organs such as the heart and kidney. Defective lysosomal alpha-galactosidase A (Gla) is responsible for excessive Gb3 accumulation, and one cell sensitive to the effects of Gb3 accumulation is vascular endothelium. Endothelial dysfunction is associated with Fabry disease and excessive cellular Gb3. We have previously demonstrated that excessive vascular Gb3 in a mouse model of Fabry disease, the Gla knockout (Gla -/0) mouse, has abnormal vascular function, which includes abnormal endothelium-dependent contractions, a vascular phenomenon known to involve cyclo-oxygenase (COX). Therefore we hypothesized that the vasculopathy in...</description>
            <author>Am J Physiol Heart C...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2176450</comments>
            <pubDate>Fri, 06 Feb 2009 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">2176450</guid>        </item>
        <item>
            <title>Activation of NTS A2a adenosine receptors differentially resets baroreflex control of renal vs. adrenal sympathetic nerve activity.</title>
            <link>http://www.medworm.com/index.php?rid=2176449&amp;cid=s_29164_7_f&amp;fid=29164&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19202001%26dopt%3DAbstract</link>
            <description>Authors: Ichinose TK, O'Leary DS, Scislo TJ
    The role of NTS A2a adenosine receptors in baroreflex mechanisms is controversial. Stimulation of these receptors releases glutamate within the NTS and elicits baroreflex like decreases in mean arterial pressure (MAP), heart rate (HR) and renal sympathetic nerve activity (RSNA), whereas inhibition of these receptors attenuates HR baroreflex responses. In contrast, stimulation of NTS A2a adenosine receptors increases preganglionic adrenal sympathetic nerve activity (pre-ASNA) and the depressor and sympathoinhibitory responses are not markedly affected by sinoaortic denervation and blockade of NTS glutamatergic transmission. To elucidate the role of NTS A2a adenosine receptors in baroreflex function we compared full baroreflex stimulus-response...</description>
            <author>Am J Physiol Heart C...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2176449</comments>
            <pubDate>Fri, 06 Feb 2009 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">2176449</guid>        </item>
        <item>
            <title>Transient opening of mitochondrial permeability transition pore by reactive oxygen species protects myocardium from ischemia/reperfusion injury.</title>
            <link>http://www.medworm.com/index.php?rid=2176448&amp;cid=s_29164_7_f&amp;fid=29164&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19202002%26dopt%3DAbstract</link>
            <description>Authors: Saotome M, Katoh H, Yaguchi Y, Tanaka T, Urushida T, Satoh H, Hayashi H
    Reactive oxygen species (ROS) production during ischemia/reperfusion (I/R) is thought to be a critical factor for myocardial injury. However a small amount of ROS during the ischemic preconditioning (IPC) may provide a signal for cardioprotection. We have previously reported that the repetitive pretreatment of a small amount of ROS (hydrogen peroxide; H2O2, 2 microM) mimicked the IPC-induced cardioprotection in the Langendorff-perfused rat hearts. We further investigated the mechanisms of the ROS-induced cardioprotection against I/R injury, and tested the hypothesis whether it could mediate the mPTP opening. The Langendorff-perfused rat hearts were subjected to 35 min ischemia and 40 min reperfusion, and t...</description>
            <author>Am J Physiol Heart C...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2176448</comments>
            <pubDate>Fri, 06 Feb 2009 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">2176448</guid>        </item>
        <item>
            <title>Cellular preservation therapy in acute myocardial infarction.</title>
            <link>http://www.medworm.com/index.php?rid=2176447&amp;cid=s_29164_7_f&amp;fid=29164&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19202003%26dopt%3DAbstract</link>
            <description>CELLULAR PRESERVATION THERAPY IN ACUTE MYOCARDIAL INFARCTION.
    Am J Physiol Heart Circ Physiol. 2009 Feb 6;
    Authors: Abbate A, Biondi-Zoccai GG, Van Tassell BW, Baldi A
    N/A Key words: acute myocardial infarction, heart failure, apoptosis, inflammation.
    PMID: 19202003 [PubMed - as supplied by publisher] (Source: Am J Physiol Heart C...)</description>
            <author>Am J Physiol Heart C...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2176447</comments>
            <pubDate>Fri, 06 Feb 2009 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">2176447</guid>        </item>
        <item>
            <title>Letter to the editor: &quot;Does baroreflex unloading decrease limb venous compliance in women?&quot;.</title>
            <link>http://www.medworm.com/index.php?rid=2140089&amp;cid=s_29164_7_f&amp;fid=29164&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19171848%26dopt%3DAbstract</link>
            <description>Authors: Monahan KD
    
    PMID: 19171848 [PubMed - in process] (Source: Am J Physiol Heart C...)</description>
            <author>Am J Physiol Heart C...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2140089</comments>
            <pubDate>Thu, 29 Jan 2009 04:43:12 +0100</pubDate>
            <guid isPermaLink="false">2140089</guid>        </item>
        <item>
            <title>Reply to &quot;Letter to the Editor: 'Does baroreflex unloading decrease limb venous compliance in women?'&quot;.</title>
            <link>http://www.medworm.com/index.php?rid=2140088&amp;cid=s_29164_7_f&amp;fid=29164&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19171849%26dopt%3DAbstract</link>
            <description>Authors: Krabbendam I, Scholten R, Spaanderman ME
    
    PMID: 19171849 [PubMed - in process] (Source: Am J Physiol Heart C...)</description>
            <author>Am J Physiol Heart C...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2140088</comments>
            <pubDate>Thu, 29 Jan 2009 04:43:08 +0100</pubDate>
            <guid isPermaLink="false">2140088</guid>        </item>
        <item>
            <title>Sympathetic Neural Responses to Mental Stress: Responders, Nonresponders and Sex Differences.</title>
            <link>http://www.medworm.com/index.php?rid=2136492&amp;cid=s_29164_7_f&amp;fid=29164&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19168718%26dopt%3DAbstract</link>
            <description>In conclusion, our results demonstrate marked differences in MSNA responses to mental stress and a disassociation between MSNA and BP responses to mental stress, suggesting complex patterns of vascular responsiveness during mental stress. Key words: autonomic nervous system, blood pressure, mental arithmetic, muscle sympathetic nerve activity.
    PMID: 19168718 [PubMed - as supplied by publisher] (Source: Am J Physiol Heart C...)</description>
            <author>Am J Physiol Heart C...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2136492</comments>
            <pubDate>Fri, 23 Jan 2009 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">2136492</guid>        </item>
        <item>
            <title>Sp1-Dependent Activation of KLF4 is Required for PDGF-BB-Induced Phenotypic Modulation of Smooth Muscle.</title>
            <link>http://www.medworm.com/index.php?rid=2136491&amp;cid=s_29164_7_f&amp;fid=29164&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19168719%26dopt%3DAbstract</link>
            <description>Authors: Deaton RA, Gan Q, Owens GK
    There is clear evidence that phenotypic modulation of smooth muscle cells (SMCs) contributes to the pathophysiology of vascular disease. Phenotypic modulation refers to the unique ability of SMCs to alter their phenotype in response to extracellular stimuli and is hallmarked by loss of SMC marker gene expression. The transcription factor KLF4 is a known powerful negative regulator of SMC marker gene expression that works, in part, by decreasing expression of the SRF co-factor, myocardin. KLF4 is not expressed in healthy adult SMCs but is increased in SMCs in response to vascular injury in vivo or PDGF-BB treatment in vitro. The aim of the present study was to determine the molecular mechanisms that regulate expression of KLF4 in phenotypically modula...</description>
            <author>Am J Physiol Heart C...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2136491</comments>
            <pubDate>Fri, 23 Jan 2009 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">2136491</guid>        </item>
        <item>
            <title>Properties and Ionic Mechanisms of Action Potential Adaptation, Restitution and Accommodation in Canine Epicardium.</title>
            <link>http://www.medworm.com/index.php?rid=2136490&amp;cid=s_29164_7_f&amp;fid=29164&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19168720%26dopt%3DAbstract</link>
            <description>Authors: Decker KF, Heijman J, Silva JR, Hund TJ, Rudy Y
    Computational models of cardiac myocytes are important tools for understanding ionic mechanisms of arrhythmia. This work presents a new model of the canine epicardial myocyte that reproduces a wide range of experimentally observed rate dependent behaviors in cardiac cell and tissue, including action potential duration (APD) adaptation, restitution and accommodation. Model behavior depends on updated formulations for the 4-AP sensitive transient outward current (Ito1), the slow component of the delayed rectifier potassium current (IKs), the L-type Ca(2+) channel (ICa,L) and the sodium-potassium pump (INaK) fit to data from canine ventricular myocytes. We find that Ito1 plays a limited role in potentiating peak ICa,L and sarcoplasm...</description>
            <author>Am J Physiol Heart C...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2136490</comments>
            <pubDate>Fri, 23 Jan 2009 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">2136490</guid>        </item>
        <item>
            <title>Interaction of vascular smooth muscle cells and monocytes by soluble factors synergistically enhances interleukin-6 and MCP-1 production.</title>
            <link>http://www.medworm.com/index.php?rid=2136489&amp;cid=s_29164_7_f&amp;fid=29164&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19168721%26dopt%3DAbstract</link>
            <description>Authors: Chen L, Frister A, Wang S, Ludwig A, Behr H, Pippig S, Li B, Simm A, Hofmann B, Pilowski C, Koch S, Buerke M, Rose-John S, Werdan K, Loppnow H
    Inflammatory mechanisms contribute to atherogenesis. Monocyte chemoattractant protein-1 (MCP-1) and interleukin-6 (IL-6) are potent mediators of inflammation. Both contribute to early atherogenesis by luring monocytes and regulating cell functions in the vessel wall. MCP-1 and IL-6 production resulting from interaction of invading monocytes with local vessel wall cells may accelerate atherosclerosis. We investigated the influence of the interaction of human vascular smooth muscle cells (SMC) with human mononuclear cells (MNC) or monocytes on the IL-6 and MCP-1 production in a coculture model. Interaction synergistically enhanced IL-6 an...</description>
            <author>Am J Physiol Heart C...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2136489</comments>
            <pubDate>Fri, 23 Jan 2009 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">2136489</guid>        </item>
        <item>
            <title>Inhibition of Integrin {alpha}V{beta}3 Prevents Urokinase Plasminogen Activator -Mediated Impairment of Cerebrovasodilation After Cerebral Hypoxia/Ischemia.</title>
            <link>http://www.medworm.com/index.php?rid=2136488&amp;cid=s_29164_7_f&amp;fid=29164&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19168722%26dopt%3DAbstract</link>
            <description>This study investigated the role of integrin alphaVbeta3, in uPA-mediated impairment of cerebrovasodilation after H/I in piglets equipped with a closed cranial window. Pial artery dilation induced by hypercapnia (pCO2 75 mm Hg) and hypotension (mean arterial blood pressure decreased by 45%) was blunted after H/I, reversed to vasconstriction in piglets treated with uPA (10-7 M), a concentration observed in CSF after H/I, but reverted to dilation no different than pre-insult in piglets administered an anti alphaVbeta3 antibody (10 ng/ml) in addition to uPA (26 +/- 1, 9 +/- 1, -10 +/- 3, and 22 +/- 3 % for hypercapnia before H/I, after H/I, after H/I with uPA, and after H/I with combined uPA and anti-alphaVbeta3 antibody, respectively). Responses to isoproterenol were unchanged after H/I and ...</description>
            <author>Am J Physiol Heart C...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2136488</comments>
            <pubDate>Fri, 23 Jan 2009 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">2136488</guid>        </item>
        <item>
            <title>HYDROGEN SULFIDE TRIGGERS LATE PHASE PRECONDITIONING IN POSTISCHEMIC SMALL INTESTINE BY AN NO- AND p38 MAPK-DEPENDENT MECHANISM.</title>
            <link>http://www.medworm.com/index.php?rid=2136487&amp;cid=s_29164_7_f&amp;fid=29164&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19168723%26dopt%3DAbstract</link>
            <description>Authors: Yusof M, Kamada K, Kalogeris T, Gaskin FS, Korthuis RJ
    Hydrogen sulfide (H2S) is one of three endogenous gases, along with carbon monoxide (CO) and nitric oxide (NO), that exerts a variety of important vascular actions in vivo. Although it has been demonstrated that CO or NO can trigger the development of a preconditioned phenotype in postischemic tissues, it is unclear whether H2S may also induce protection in organs subsequently exposed to ischemia/reperfusion (I/R). Thus, we postulated that preconditioning with an exogenous H2S donor (NaHS-PC) would inhibit leukocyte rolling (LR) and adhesion (LA) induced by subsequent exposure to I/R. We used intravital microscopic techniques to demonstrate that NaHS-PC 24 hrs, but not 1 hr, prior to I/R causes postcapillary venules to shi...</description>
            <author>Am J Physiol Heart C...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2136487</comments>
            <pubDate>Fri, 23 Jan 2009 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">2136487</guid>        </item>
        <item>
            <title>Coronary Blood Flow Responses to Physiological Stress in Humans.</title>
            <link>http://www.medworm.com/index.php?rid=2136486&amp;cid=s_29164_7_f&amp;fid=29164&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19168724%26dopt%3DAbstract</link>
            <description>Authors: Momen A, Mascarenhas V, Gahremanpour A, Gao Z, Moradkhan R, Kunselman A, Boehmer JP, Sinoway LI, Leuenberger UA
    Animal reports suggest that reflex activation of cardiac sympathetic nerves can evoke coronary vasoconstriction. Conversely, physiologic stress may induce coronary vasodilation to meet an increased metabolic demand. Whether the sympathetic nervous system can modulate coronary vasomotor tone in response to stress in humans is unclear. Coronary blood velocity (CBV), an index of coronary blood flow, can be measured in humans by noninvasive duplex ultrasound. We studied 11 healthy volunteers and measured beat-by-beat changes in CBV, blood pressure, and heart rate during: a) static handgrip for 20 s at 10% and 70% of maximal voluntary contraction; b) lower body negative p...</description>
            <author>Am J Physiol Heart C...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2136486</comments>
            <pubDate>Fri, 23 Jan 2009 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">2136486</guid>        </item>
        <item>
            <title>Impaired hemodynamics and endothelial vasomotor function via endoperoxide-mediated vasoconstriction in the carotid artery of spontaneously hypertensive rats.</title>
            <link>http://www.medworm.com/index.php?rid=2136485&amp;cid=s_29164_7_f&amp;fid=29164&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19168725%26dopt%3DAbstract</link>
            <description>We report that mean, maximal systolic, and diastolic blood flow were reduced in SHR vs. WKY CCA, as was vascular conductance. Pressure was augmented in SHR CCA and accompanied by late systolic flow augmentation so that total flow during systole was indeed no different between strains, possibly explained by earlier lower body wave reflection. While acetylcholine (ACh) stimulation in isolated precontracted WKY CCA caused a robust nitric oxide (NO)-mediated vasorelaxation, endothelium-dependent, cyclooxygenase (COX)-mediated contractile activity stimulated by high [ACh] impaired NO- and non-NO/non-COX-mediated vasorelaxation in precontracted SHR CCA. In quiescent CCA, this endothelium-dependent contractile response was COX-1- and thromboxane-prostanoid receptor-mediated, and modulated by the ...</description>
            <author>Am J Physiol Heart C...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2136485</comments>
            <pubDate>Fri, 23 Jan 2009 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">2136485</guid>        </item>
        <item>
            <title>Muscle Ring Finger-1 (MuRF1) Mediates Cardiac Atrophy in vivo.</title>
            <link>http://www.medworm.com/index.php?rid=2136484&amp;cid=s_29164_7_f&amp;fid=29164&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19168726%26dopt%3DAbstract</link>
            <description>Authors: Willis MS, Rojas M, Li L, Selzman CH, Tang RH, Stansfield WE, Rodriguez JE, Glass D, Patterson C
    Pathologic cardiac hypertrophy, induced by various etiologies such as high blood pressure and aortic stenosis, develops in response to increased afterload and represents a common intermediary in the development of heart failure. Understandably then, the reversal of pathologic cardiac hypertrophy is associated with a significant reduction in cardiovascular event risk, and represents an important yet underdeveloped target of therapeutic research. Recently we determined that muscle ring finger-1 (MuRF1), a muscle-specific protein, inhibits the development of experimentally-induced pathologic cardiac hypertrophy. We now demonstrate that therapeutic cardiac atrophy induced in patients a...</description>
            <author>Am J Physiol Heart C...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2136484</comments>
            <pubDate>Fri, 23 Jan 2009 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">2136484</guid>        </item>
        <item>
            <title>NADPH Oxidase Contributes to Coronary Endothelial Dysfunction in the Failing Heart.</title>
            <link>http://www.medworm.com/index.php?rid=2136483&amp;cid=s_29164_7_f&amp;fid=29164&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19168727%26dopt%3DAbstract</link>
            <description>This study tested the hypothesis that NADPH oxidase is a significant source of ROS that contributes to coronary endothelial dysfunction in the failing heart. Congestive heart failure (CHF) was produced in 6 dogs by ventricular pacing at 240 beats/min for 4 weeks. Studies were performed at rest and during treadmill exercise during control conditions and after NADPH oxidase inhibition with apocynin (4 mg/kg, iv). Apocynin caused no significant changes in heart rate, aortic pressure, LV systolic pressure, LVEDP or LV dP/dtmax at rest or during exercise in either normal or CHF dogs. Apocynin caused no change in coronary blood flow (CBF) in normal dogs, but increased CBF at rest and during exercise in animals with CHF (p&amp;lt;0.05). Intracoronary acetylcholine caused dose dependent increases of C...</description>
            <author>Am J Physiol Heart C...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2136483</comments>
            <pubDate>Fri, 23 Jan 2009 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">2136483</guid>        </item>
        <item>
            <title>Suppression of Nitrosative and Oxidative Stress to Reduce Cardiac Allograft Vasculopathy.</title>
            <link>http://www.medworm.com/index.php?rid=2136482&amp;cid=s_29164_7_f&amp;fid=29164&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19168728%26dopt%3DAbstract</link>
            <description>Authors: Hasegawa T, Iwanaga K, Hultquist DE, Liao H, Visovatti SH, Pinsky DJ
    Oxidant injury occurs when an organ is severed from its native blood supply and then reperfused, and continues during subsequent periods of immune attack. Experiments here test the hypothesis that an antioxidant given only in the peri-reperfusion period protects against not only oxidative but also nitrosative stress, leading to reduced vasculopathy long after cardiac allotransplantation. Experiments were performed using a murine heterotopic cardiac transplantation model. An antioxidant, in the form of intraperitoneal high-dose riboflavin, was given to recipients during the initial 3 days after transplantation. Antioxidant-treated mice showed significantly longer graft survival than control mice. At 4 hours af...</description>
            <author>Am J Physiol Heart C...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2136482</comments>
            <pubDate>Fri, 23 Jan 2009 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">2136482</guid>        </item>
        <item>
            <title>Peroxide Generation by p47phox-Src Activation of Nox2 Has a Key Role in Protein Kinase C-Induced Arterial Smooth Muscle Contraction.</title>
            <link>http://www.medworm.com/index.php?rid=2136481&amp;cid=s_29164_7_f&amp;fid=29164&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19168729%26dopt%3DAbstract</link>
            <description>Authors: Gupte SA, Kaminski PM, George S, Kouznestova L, Olson SC, Matthew R, Hintze TH, Wolin MS
    Protein kinase C (PKC) stimulation of NAD(P)H oxidases (Nox) is an important component of multiple vascular disease processes, however, the relationship between oxidase activation and the regulation vascular smooth muscle contraction by PKC remains poorly understood. Therefore, we examined the signaling cascade of PKC-elicited Nox activation and the role of superoxide and hydrogen peroxide in mediating PKC induced vascular contraction. Endothelium-denuded bovine coronary arteries showed a PKC-dependent basal production of lucigenin (5 mM)-detected Nox oxidase-derived superoxide, which was stimulated 4-fold by PKC activation with 10 microM phorbol 12,13-dibutyrate (PDBu). PDBu appeared to i...</description>
            <author>Am J Physiol Heart C...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2136481</comments>
            <pubDate>Fri, 23 Jan 2009 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">2136481</guid>        </item>
        <item>
            <title>Is EPO behind Maladaptive Anemic Heart Failure?</title>
            <link>http://www.medworm.com/index.php?rid=2136480&amp;cid=s_29164_7_f&amp;fid=29164&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19168730%26dopt%3DAbstract</link>
            <description>Authors: Gao E, Koch WJ
    This is an editorial - no abstract Key words: anemia, erythropoietin, heart failure, hypertrophy.
    PMID: 19168730 [PubMed - as supplied by publisher] (Source: Am J Physiol Heart C...)</description>
            <author>Am J Physiol Heart C...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2136480</comments>
            <pubDate>Fri, 23 Jan 2009 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">2136480</guid>        </item>
        <item>
            <title>Cytokines are produced locally by myocytes in rat skeletal muscle during endotoxemia.</title>
            <link>http://www.medworm.com/index.php?rid=2119077&amp;cid=s_29164_7_f&amp;fid=29164&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19151248%26dopt%3DAbstract</link>
            <description>Authors: Borge BA, Kalland KH, Olsen S, Bletsa A, Berggreen E, Wiig H
    Cytokines act as chemical mediators during the inflammatory process. Measurements of cytokine level in tissue have previously been performed in homogenized tissue, and the true concentrations in native interstitial fluid (ISF), i.e. the compartment where cytokines exert their biologically active role, have remained unknown. The role of skeletal muscle myocytes as a source for cytokines during endotoxemia was explored by collecting muscle ISF using a wick method, and the level of 14 cytokines in ISF and plasma was related to corresponding changes in mRNA level to reveal any potential discrepancies between gene expression and protein release of cytokines to ISF. The majority of investigated cytokines were elevated in m...</description>
            <author>Am J Physiol Heart C...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2119077</comments>
            <pubDate>Fri, 16 Jan 2009 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">2119077</guid>        </item>
        <item>
            <title>Angiotensin II, mitochondria, cytoskeletal and extracellular matrix connections: an integrating viewpoint.</title>
            <link>http://www.medworm.com/index.php?rid=2119076&amp;cid=s_29164_7_f&amp;fid=29164&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19151249%26dopt%3DAbstract</link>
            <description>Authors: de Cavanagh EM, Ferder M, Inserra F, Ferder L
    Malfunctioning mitochondria strongly participate in the pathogenesis of cardiovascular damage associated with hypertension, and other disease conditions. Eukaryotic cells move, assume their shape, resist mechanical stress, accommodate their internal constituents, and transmit signals by relying on the constant remodeling of cytoskeleton filaments. Mitochondrial ATP is needed to support cytoskeletal dynamics. Conversely, mitochondria need to interact with cytoskeletal elements to achieve normal motility, morphology, localization and function. Extracellular matrix (ECM) quantity and quality influences cellular growth, differentiation, morphology, survival, and mobility. Mitochondria can sense ECM composition changes, and changes in m...</description>
            <author>Am J Physiol Heart C...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2119076</comments>
            <pubDate>Fri, 16 Jan 2009 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">2119076</guid>        </item>
        <item>
            <title>Reactive Oxygen Species and the Control of Vascular Function.</title>
            <link>http://www.medworm.com/index.php?rid=2119075&amp;cid=s_29164_7_f&amp;fid=29164&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19151250%26dopt%3DAbstract</link>
            <description>This article summarizes perspectives on how reactive oxygen species (ROS) and redox signaling mechanisms participate in regulating vascular smooth muscle function that have resulted from our studies over the past 25 years in areas including oxygen sensing and the regulation of cGMP production by soluble guanylate cyclase (sGC) that were presented in the Robert M. Berne Distinguished Lectureship at the 2008 Experimental Biology Meeting. It considers mechanisms controlling the activity of sources of ROS including Nox oxidases and mitochondria by physiological stimuli, vascular diseases processes, and metabolic mechanisms linked to NAD(P)H redox and hypoxia. Metabolic interactions of individual ROS such as hydrogen peroxide with cellular peroxide metabolizing enzymes are viewed as some of the...</description>
            <author>Am J Physiol Heart C...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2119075</comments>
            <pubDate>Fri, 16 Jan 2009 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">2119075</guid>        </item>
        <item>
            <title>Stress phase-angle depicts differences in coronary artery hemodynamics due to changes in flow and geometry after percutaneous coronary intervention.</title>
            <link>http://www.medworm.com/index.php?rid=2119074&amp;cid=s_29164_7_f&amp;fid=29164&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19151251%26dopt%3DAbstract</link>
            <description>Authors: Torii R, Wood NB, Hadjiloizou N, Dowsey AW, Wright A, Hughes AD, Davies J, Francis DP, Mayet J, Yang GZ, Thom SA, Xu XY
    The effects of changes in flow velocity waveform and arterial geometry before and after percutaneous coronary intervention (PCI) in a right coronary artery (RCA) were investigated using computational fluid dynamics. An RCA from a patient with a stenosis was reconstructed based on multislice CT images. A non-stenosed model, simulating the same RCA after PCI, was also constructed. Blood flows in the RCA models were simulated using pulsatile flow waveforms acquired with an intravascular ultrasound Doppler probe in the RCA of a patient undergoing PCI. It was found that differences in the waveforms before and after PCI did not affect time-averaged wall shear stres...</description>
            <author>Am J Physiol Heart C...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2119074</comments>
            <pubDate>Fri, 16 Jan 2009 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">2119074</guid>        </item>
        <item>
            <title>Combined therapy with cardioprotective cytokine administration and anti-apoptotic gene transfer in postinfarction heart failure.</title>
            <link>http://www.medworm.com/index.php?rid=2119073&amp;cid=s_29164_7_f&amp;fid=29164&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19151252%26dopt%3DAbstract</link>
            <description>Authors: Okada H, Takemura G, Kosai KI, Tsujimoto A, Esaki M, Takahashi T, Nagano S, Kanamori H, Miyata S, Li Y, Ohno T, Maruyama R, Ogino A, Li L, Nakagawa M, Nagashima K, Fujiwara T, Fujiwara H, Minatoguchi S
    We hypothesized that therapy comprised of anti-apoptotic soluble Fas (sFas) gene transfer combined with administration of the cardioprotective cytokine granulocyte colony-stimulating factor (G-CSF) would markedly mitigate cardiac remodeling and dysfunction following myocardial infarction (MI). On the 3rd day after MI induced by ligating the left coronary artery in mice, 4 different treatments were initiated: saline injection (Group C, n=26); G-CSF administration (Group G, n=27); adenoviral transfer of sFas gene (Group F, n=26); and the latter 2 together (Group G+F, n=26). Four w...</description>
            <author>Am J Physiol Heart C...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2119073</comments>
            <pubDate>Fri, 16 Jan 2009 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">2119073</guid>        </item>
        <item>
            <title>The Role of Angiotensin II and Oxidative Stress in Vascular Insulin Resistance Linked to Hypertension.</title>
            <link>http://www.medworm.com/index.php?rid=2119072&amp;cid=s_29164_7_f&amp;fid=29164&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19151253%26dopt%3DAbstract</link>
            <description>Authors: Zhou MS, Schulman IH, Raij L
    Insulin activation of the phosphatidylinositol 3-kinase (PI3K) pathway stimulates glucose uptake in peripheral tissues and synthesis of nitric oxide (NO) in the endothelium. Insulin resistance (IR) and hypertension frequently coexist particularly among individuals with salt-sensitive (SS) hypertension. The mechanisms underlying this association are poorly understood. We investigated these mechanisms in a model of SS hypertension in which we have previously shown that endothelial dysfunction is mediated by superoxide (O2(-)) linked to local angiotensin II. Dahl SS rats were fed for 6 weeks a normal salt (NS, 0.5% NaCl) or high salt (HS, 4% NaCl) diet, HS plus angiotensin II type 1 receptor (AT1R) blocker candesartan (ARB, 10 mg/kg/day), or HS plus a...</description>
            <author>Am J Physiol Heart C...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2119072</comments>
            <pubDate>Fri, 16 Jan 2009 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">2119072</guid>        </item>
        <item>
            <title>Elevated cyclic stretch alters matrix remodeling in aortic valve cusps - implications for degenerative aortic valve disease?</title>
            <link>http://www.medworm.com/index.php?rid=2119071&amp;cid=s_29164_7_f&amp;fid=29164&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19151254%26dopt%3DAbstract</link>
            <description>Conclusions: Elevated mechanical stretch on aortic valve cusps may detrimentally alter proteolytic enzyme expression and activity in valve cells. This may trigger a cascade of events leading to accelerated valve degeneration and disease progression. Key words: Remodeling, MMP, Cathepsin, Cyclic Stretch.
    PMID: 19151254 [PubMed - as supplied by publisher] (Source: Am J Physiol Heart C...)</description>
            <author>Am J Physiol Heart C...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2119071</comments>
            <pubDate>Fri, 16 Jan 2009 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">2119071</guid>        </item>
        <item>
            <title>Increased Vascular Angiotensin Type 2 Receptor Expression and NOS-Mediated Mechanisms of Vascular Relaxation in Pregnant Rats.</title>
            <link>http://www.medworm.com/index.php?rid=2119070&amp;cid=s_29164_7_f&amp;fid=29164&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19151255%26dopt%3DAbstract</link>
            <description>Authors: Stennett AK, Qiao X, Falone AE, Koledove VV, Khalil RA
    Angiotensin II (AngII) activates both AT1R and AT2R. Although the role of AT1R in vascular contraction is well-documented, the role of AT2R in vascular relaxation, particularly during pregnancy, is less clear. It was hypothesized that the decreased BP and vasoconstriction during pregnancy was, at least in part, due to changes in AT2R amount, distribution and/or postreceptor mechanisms of vascular relaxation. Systolic BP was measured in virgin and pregnant (day 19) Sprague-Dawley rats. Isometric contraction/relaxation was measured in isolated aortic rings, and NO production was measured using DAF-FM fluorescence. AT1R and AT2R mRNA expression and protein amount were measured in tissue homogenate using real-time RT-PCR and W...</description>
            <author>Am J Physiol Heart C...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2119070</comments>
            <pubDate>Fri, 16 Jan 2009 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">2119070</guid>        </item>
        <item>
            <title>Suppressed Hindlimb Perfusion in Rac2-/- and Nox2-/- Mice Does Not Result from Impaired Collateral Growth.</title>
            <link>http://www.medworm.com/index.php?rid=2119069&amp;cid=s_29164_7_f&amp;fid=29164&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19151256%26dopt%3DAbstract</link>
            <description>In this study, we utilized Rac2-/- and Nox2-/- mice with a novel method of identifying primary hindlimb collaterals to investigate the hypothesis that collateral growth requires these molecules. When initial studies performed with femoral ligation demonstrated similar perfusion and collateral growth in the Rac2-/- and C57BL/6 Wild-type (BL6), subsequent studies were performed with a more severe ischemia model, femoral artery excision. After femoral excision, tissue perfusion was suppressed in Rac2 -/- relative to BL6 mice. Histological assessment of ischemic injury including necrotic and regenerated muscle fibers and lipid and collagen deposition demonstrated greater injury in the Rac2 -/-. The diameters of primary collaterals identified during Microfil(R) injection with intravital microsc...</description>
            <author>Am J Physiol Heart C...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2119069</comments>
            <pubDate>Fri, 16 Jan 2009 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">2119069</guid>        </item>
        <item>
            <title>Endothelin Downregulates SERCA2 Gene and Protein Expression in Adult Rat Ventricular Myocytes: Regulation by Pertussis Toxin-Sensitive Gi Protein and cAMP.</title>
            <link>http://www.medworm.com/index.php?rid=2119068&amp;cid=s_29164_7_f&amp;fid=29164&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19151257%26dopt%3DAbstract</link>
            <description>Authors: Hilal-Dandan R, He H, Martin JL, Brunton LL, Dillmann WH
    Down regulation of the sarcoplasmic reticulum calcium ATPase (SERCA2) is associated with diastolic dysfunction in the failing heart. Elevated plasma endothelin-1 (ET) levels are correlated with congestive heart failure suggesting that ET may play a pathophysiological role. We have investigated the ability of ET to regulate SERCA2 gene expression in isolated adult rat ventricular myocytes. We find that ET enhances net protein synthesis by ~ 40% but significantly downregulates SERCA2 mRNA expression, time dependently, by ~30-50%, and the expression of SERCA2 protein by ~ 50%. In myoyctes, ET binds to ETA receptor that couples to Gq and Gi proteins. Inhibition of Gq-PLC induced phosphoinositide (PI) hydrolysis with U7-3122(...</description>
            <author>Am J Physiol Heart C...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2119068</comments>
            <pubDate>Fri, 16 Jan 2009 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">2119068</guid>        </item>
        <item>
            <title>PPAR-alpha activation protects the type 2 diabetic myocardium against ischemia-reperfusion injury: involvement of the PI3-kinase/Akt and NO pathway.</title>
            <link>http://www.medworm.com/index.php?rid=2119067&amp;cid=s_29164_7_f&amp;fid=29164&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19151258%26dopt%3DAbstract</link>
            <description>Authors: Bulhak AA, Jung C, Ostenson CG, Lundberg JO, Sj&amp;#xF6;quist PO, Pernow J
    Several clinical studies have shown beneficial cardiovascular effects of fibrates in patients with diabetes and insulin resistance. Ligands of peroxisome proliferator-activated receptor alpha (PPAR-alpha) reduce ischemia-reperfusion injury in non-diabetic animals. We hypothesized that activation of PPAR-alpha would exert cardioprotection in type 2 diabetic Goto-Kakizaki (GK) rats, involving mechanisms related to nitric oxide (NO) production via the phosphatidylinositol 3-kinase (PI3-K)/Akt pathway. GK rats and age-matched Wistar rats (n&amp;gt;/=7) were given either 1) the PPAR-alpha agonist WY 14643, 2) Dimethylsulphoxide (DMSO), 3) WY and the NO synthase inhibitor N-nitro-L-arginine (L-NNA), 4) L-NNA, 5) WY ...</description>
            <author>Am J Physiol Heart C...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2119067</comments>
            <pubDate>Fri, 16 Jan 2009 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">2119067</guid>        </item>
        <item>
            <title>Beating to time: calcium clocks, voltage clocks and cardiac pacemaker activity.</title>
            <link>http://www.medworm.com/index.php?rid=2119066&amp;cid=s_29164_7_f&amp;fid=29164&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19151259%26dopt%3DAbstract</link>
            <description>Authors: Eisner DA, Cerbai E
    not needed Key words: calcium, pacemaker.
    PMID: 19151259 [PubMed - as supplied by publisher] (Source: Am J Physiol Heart C...)</description>
            <author>Am J Physiol Heart C...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2119066</comments>
            <pubDate>Fri, 16 Jan 2009 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">2119066</guid>        </item>
        <item>
            <title>Synergism of coupled subsarcolemmal Ca2+ clocks and sarcolemmal voltage clocks confers robust and flexible pacemaker function in a novel pacemaker cell model.</title>
            <link>http://www.medworm.com/index.php?rid=2099670&amp;cid=s_29164_7_f&amp;fid=29164&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19136600%26dopt%3DAbstract</link>
            <description>Conclusion: The Ca(2+)clock is a new critical dimension in SANC function. A synergism of the coupled function of Ca(2+) and membrane clocks confers fail-safe SANC operation at greatly varying rates. Key words: Calcium, sarcoplasmic reticulum, ion channels, numerical modeling.
    PMID: 19136600 [PubMed - as supplied by publisher] (Source: Am J Physiol Heart C...)</description>
            <author>Am J Physiol Heart C...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2099670</comments>
            <pubDate>Fri, 09 Jan 2009 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">2099670</guid>        </item>
        <item>
            <title>20-hete increases survival and decreases apoptosis in pulmonary arteries and pulmonary artery endothelial cells.</title>
            <link>http://www.medworm.com/index.php?rid=2099669&amp;cid=s_29164_7_f&amp;fid=29164&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19136601%26dopt%3DAbstract</link>
            <description>20-HETE INCREASES SURVIVAL AND DECREASES APOPTOSIS IN PULMONARY ARTERIES AND PULMONARY ARTERY ENDOTHELIAL CELLS.
    Am J Physiol Heart Circ Physiol. 2009 Jan 9;
    Authors: Dhanasekaran A, Bodiga S, Gruenloh SK, Gao Y, Dunn LK, Falck JR, Buonaccorsi JN, Medhora MM, Jacobs ER
    20-hydroxyeicosatetraenoic acid (20-HETE) is an endogenous cytochrome P450 product present in vascular smooth muscle and uniquely located in the vascular endothelium of pulmonary arteries (PAs). 20-HETE enhances reactive oxygen species (ROS) production of bovine pulmonary artery endothelial cells (BPAECs) in an NADPH oxidase dependent manner, and is postulated to promote angiogenesis via activation of this pathway in systemic vascular beds. We tested the capacity of 20-HETE or a stable analog of this compound 20-...</description>
            <author>Am J Physiol Heart C...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2099669</comments>
            <pubDate>Fri, 09 Jan 2009 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">2099669</guid>        </item>
        <item>
            <title>Temporal Changes in Expression of Connexin-43 after Load-induced Hypertrophy In Vitro.</title>
            <link>http://www.medworm.com/index.php?rid=2099668&amp;cid=s_29164_7_f&amp;fid=29164&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19136602%26dopt%3DAbstract</link>
            <description>Authors: Bupha-Intr T, Haizlip KM, Janssen PM
    Upon remodeling of the ventricle after a provoking stimulus, such as hypertension, connections between adjacent myocytes may need to be &quot;reformatted&quot; to preserve synchronization of excitation of the remodeling heart. In the mammalian heart, the protein connexin forms the gap junctions that allow electrical and chemical signaling communication between neighboring cells. We aim to elucidate if mechanical load, in isolation, potentially changes the expression of connexin 43 (Cx43), the major isoform of connexin family in the ventricle, and its phosphorylation. Cx43 expression levels and contractile function of multicellular rabbit cardiac preparations were assessed in a newly developed in vitro system that allows for the study of the transitio...</description>
            <author>Am J Physiol Heart C...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2099668</comments>
            <pubDate>Fri, 09 Jan 2009 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">2099668</guid>        </item>
        <item>
            <title>Respiratory Modulation of Heart Sound Morphology.</title>
            <link>http://www.medworm.com/index.php?rid=2099667&amp;cid=s_29164_7_f&amp;fid=29164&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19136603%26dopt%3DAbstract</link>
            <description>Authors: Amit G, Shukha K, Gavriely N, Intrator N
    Heart sounds, the acoustic vibrations produced by the mechanical processes of the cardiac cycle, are modulated by respiratory activity. We have used computational techniques of cluster analysis and classification to study the effects of the respiratory phase and the respiratory resistive load on the temporal and morphological properties of the first (S1) and second (S2) heart sounds, acquired from 12 healthy volunteers. Heart sounds exhibited strong morphological variability during normal respiration, and nearly no variability during apnea. The variability was shown to be periodic, with its estimated period was in good agreement with the measured duration of the respiratory cycle. Significant differences were observed between properties...</description>
            <author>Am J Physiol Heart C...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2099667</comments>
            <pubDate>Fri, 09 Jan 2009 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">2099667</guid>        </item>
        <item>
            <title>Cardiomyocytes from post-infarction failing rat hearts have improved ischemia tolerance.</title>
            <link>http://www.medworm.com/index.php?rid=2099666&amp;cid=s_29164_7_f&amp;fid=29164&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19136604%26dopt%3DAbstract</link>
            <description>Conclusion: Tolerance to hypoxia and reoxygenation surprisingly was higher in CHF than in SHAM cardiomyocytes, probably explained by lower hypoxia-mediated Na(+) accumulation and subsequent lower Ca(2+) accumulation in CHF after reoxygenation. Key words: Heart failure, ischemia, calcium, sodium.
    PMID: 19136604 [PubMed - as supplied by publisher] (Source: Am J Physiol Heart C...)</description>
            <author>Am J Physiol Heart C...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2099666</comments>
            <pubDate>Fri, 09 Jan 2009 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">2099666</guid>        </item>
        <item>
            <title>Granulocyte colony-stimulating factor protects cardiac mitochondria in the early phase of cardiac injury.</title>
            <link>http://www.medworm.com/index.php?rid=2099665&amp;cid=s_29164_7_f&amp;fid=29164&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19136605%26dopt%3DAbstract</link>
            <description>Authors: Hiraumi Y, Iwai-Kanai E, Baba S, Yui Y, Kamitsuji Y, Mizushima Y, Matsubara H, Watanabe M, Watanabe KI, Toyokuni S, Matsubara H, Nakahata T, Adachi S
    Although granulocyte colony-stimulating factor (G-CSF) reportedly plays a cardioprotective role in several models of cardiac injury, clinical use of this drug for cardiac patients has been controversial. Here, we tested the effect of G-CSF in vivo and in vitro on cardiac mitochondria, which play a key role in determining cardiac cellular fate and function. Mild stimulation of C57/BL6 mice with doxorubicin (dox)did not induce cardiac apoptosis or fibrosis, but did induce electron microscopic damages in the mitochondrial alignment of the myocardium. Cardiac catheterization or echocardiogram revealed that dox did not alter cardiac s...</description>
            <author>Am J Physiol Heart C...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2099665</comments>
            <pubDate>Fri, 09 Jan 2009 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">2099665</guid>        </item>
        <item>
            <title>The hexosamine biosynthesis inhibitor azaserine prevents endothelial inflammation and dysfunction under hyperglycemic condition through anti-oxidant effects.</title>
            <link>http://www.medworm.com/index.php?rid=2099664&amp;cid=s_29164_7_f&amp;fid=29164&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19136606%26dopt%3DAbstract</link>
            <description>In conclusion, hyperglycemia independently increases oxidative stress and HBP flux, amplifies endothelial inflammation and impairs endothelial function mainly through oxidative stress and not the HBP pathway. Azaserine protects against hyperglycemic endothelial damage through its anti-oxidant effect independently of inhibiting HBP pathway. Key words: Adhesion molecules, endothelium, glucose, O-GlcNAc.
    PMID: 19136606 [PubMed - as supplied by publisher] (Source: Am J Physiol Heart C...)</description>
            <author>Am J Physiol Heart C...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2099664</comments>
            <pubDate>Fri, 09 Jan 2009 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">2099664</guid>        </item>
        <item>
            <title>Interatrial Shunt for Chronic Pulmonary Hypertension: Differential Impact of Low-Flow versus High-Flow Shunting.</title>
            <link>http://www.medworm.com/index.php?rid=2099663&amp;cid=s_29164_7_f&amp;fid=29164&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19136607%26dopt%3DAbstract</link>
            <description>This study demonstrated that Low-Flow interatrial shunting consistently improved right atrial mechanics and systemic perfusion in subjects with CPH, while High-Flow exceeded an &quot;ideal shunt fraction&quot;. Key words: Pulmonary hypertension, Right heart failure, Atrial septostomy, Interatrial shunt.
    PMID: 19136607 [PubMed - as supplied by publisher] (Source: Am J Physiol Heart C...)</description>
            <author>Am J Physiol Heart C...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2099663</comments>
            <pubDate>Fri, 09 Jan 2009 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">2099663</guid>        </item>
        <item>
            <title>Adaptive response of the heart to long term anemia induced by iron deficiency.</title>
            <link>http://www.medworm.com/index.php?rid=2099662&amp;cid=s_29164_7_f&amp;fid=29164&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19136608%26dopt%3DAbstract</link>
            <description>Authors: Naito Y, Tsujino T, Matsumoto M, Sakoda T, Ohyanagi M, Masuyama T
    Anemia is common in patients with chronic heart failure, and an independent predictor of poor prognosis. Chronic anemia leads to left ventricular (LV) hypertrophy and heart failure, but its molecular mechanisms remain largely unknown. We investigated the mechanisms, including the molecular signaling pathway, of cardiac remodeling induced by iron deficiency anemia (IDA). Iron deficient diet was given for 20 weeks in weanling Sprague-Dawley rats to induce IDA, and these rats were studied for the evaluation of molecular mechanisms of cardiac remodeling. Iron deficient diet initially induced severe anemia, which resulted in LV hypertrophy and dilation with preserved systolic function associated with increased serum ...</description>
            <author>Am J Physiol Heart C...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2099662</comments>
            <pubDate>Fri, 09 Jan 2009 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">2099662</guid>        </item>
        <item>
            <title>Cardiac Fibroblasts Require Focal Adhesion Kinase for Normal Proliferation and Migration.</title>
            <link>http://www.medworm.com/index.php?rid=2099661&amp;cid=s_29164_7_f&amp;fid=29164&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19136609%26dopt%3DAbstract</link>
            <description>Authors: Manso AM, Kang SM, Plotnikov SV, Thievessen I, Oh J, Beggs HE, Ross RS
    Migration and proliferation of cardiac fibroblasts (CFs) play an important role in the myocardial remodeling process. While many factors have been identified that regulate CF growth and migration, less is known about the signaling mechanisms involved in these processes. Here, we utilized Cre-LoxP technology to obtain Focal Adhesion Kinase (FAK)-deficient adult mouse CFs and studied how FAK functioned in modulating cell adhesion, proliferation and migration of these cells. Treatment of FAK(flox/flox) CFs with Adeno/Cre virus caused over 70% reduction of FAK protein levels within a cell population. FAK deficient CFs showed no changes in focal adhesions, cell morphology or protein expression levels of vinculin...</description>
            <author>Am J Physiol Heart C...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2099661</comments>
            <pubDate>Fri, 09 Jan 2009 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">2099661</guid>        </item>
        <item>
            <title>Atrial natriuretic peptide increases inflammation, infarct size and mortality after experimental coronary occlusion.</title>
            <link>http://www.medworm.com/index.php?rid=2082819&amp;cid=s_29164_7_f&amp;fid=29164&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19122164%26dopt%3DAbstract</link>
            <description>Authors: Houng AK, McNamee RA, Kerner A, Sharma P, Mohamad A, Tronolone J, Reed GL
    Acute coronary artery occlusion triggers the release of atrial natriuretic peptide (ANP) from the heart. ANP affects vasodilation, natriuresis and inflammation, but the integrated biologic effects of ANP on myocardial infarction are unknown. To elucidate these effects, the left anterior coronary artery was ligated in anesthetized, ANP-deficient (ANP(-/-)) and congenic wild-type (ANP(+/+)) mice. The survival of ANP(-/-) mice was markedly better (56%) 30 days post-infarction than the survival of ANP(+/+) mice (20%, p &amp;lt; 0.01). Surviving mice were comparable initially, but ANP(-/-) mice developed more cardiac hypertrophy (p &amp;lt; 0.001) and had lower contractility indices 30 days after infarction (p &amp;lt; 0...</description>
            <author>Am J Physiol Heart C...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2082819</comments>
            <pubDate>Fri, 02 Jan 2009 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">2082819</guid>        </item>
        <item>
            <title>Phosphoinositide 3-kinase Akt signaling pathway interacts with protein kinase C{beta}2 in the regulation of physiologic developmental hypertrophy and heart function.</title>
            <link>http://www.medworm.com/index.php?rid=2082818&amp;cid=s_29164_7_f&amp;fid=29164&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19122165%26dopt%3DAbstract</link>
            <description>In this study, we examined the potential interaction between the PI3K and PKCbeta2 pathways by crossing transgenic (Tg) mice with cardiac specific expression of PKCbeta2, constitutively active PI3K and dominant negative PI3K. In caPI3K/PKCbeta2 and dnPI3K/PKCbeta2 double transgenic mice, the heart weight/body weight (HW/BW) ratios and cardiomyocyte sizes were similar to those observed in caPI3K and dnPI3K transgenic mice, respectively, suggesting that the regulation of physiologic developmental hypertrophy via modulation of cardiomyocyte size proceeds through the PI3K pathway. In addition, we observed that caPI3K/PKCbeta2 mice showed improved cardiac function while the function of dnPI3K/PKCbeta2 mice was similar to that of the PKCbeta2 group. PKCbeta2 protein levels in both dnPI3K/PKCbeta...</description>
            <author>Am J Physiol Heart C...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2082818</comments>
            <pubDate>Fri, 02 Jan 2009 05:00:00 +0100</pubDate>
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        <item>
            <title>Left ventricular regional wall curvedness and wall stress in patients with ischemic dilated cardiomyopathy.</title>
            <link>http://www.medworm.com/index.php?rid=2082817&amp;cid=s_29164_7_f&amp;fid=29164&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19122166%26dopt%3DAbstract</link>
            <description>The objective of this study was to determine the regional curvatures and wall stress based on 3D reconstructions of the LV using magnetic resonance imaging (MRI). Ten ischemic dilated cardiomyopathy (IDCM) and ten normal subjects underwent MRI scan. The former also underwent delayed gadolinium-enhancement imaging to delineate the extent of myocardial infarct. Regional curvedness (C), local radii of curvature and wall thickness were calculated. The % curvedness change (C) between end-diastole and end-systole was also calculated. In normal heart, a short-axis and long-axis 2D analysis showed a 41% +/- 11% and 45% +/- 12% increase of the mean of peak systolic wall stress between basal and apical sections, respectively. There was no significant difference, however, in peak systolic wall stress...</description>
            <author>Am J Physiol Heart C...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2082817</comments>
            <pubDate>Fri, 02 Jan 2009 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">2082817</guid>        </item>
        <item>
            <title>Lymphatic pump-conduit duality: contraction of post-nodal lymphatic vessels inhibits passive flow.</title>
            <link>http://www.medworm.com/index.php?rid=2082816&amp;cid=s_29164_7_f&amp;fid=29164&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19122167%26dopt%3DAbstract</link>
            <description>LYMPHATIC PUMP-CONDUIT DUALITY: CONTRACTION OF POST-NODAL LYMPHATIC VESSELS INHIBITS PASSIVE FLOW.
    Am J Physiol Heart Circ Physiol. 2009 Jan 2;
    Authors: Quick CM, Ngo BL, Venugopal AM, Stewart RH
    Lymphangions, the segments of lymphatic vessels between valves, exhibit structural characteristics in common with both ventricles and arteries. Although once viewed as passive conduits like arteries, it has become well-established that lymphangions can actively pump lymph against an axial pressure gradient from low-pressure tissues to the great veins of the neck. A recently-reported mathematical model, based on fundamental principles, predicted that lymphangions can transition from pump to conduit behavior when outlet pressure falls below inlet pressure. In this case, the axial pressur...</description>
            <author>Am J Physiol Heart C...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2082816</comments>
            <pubDate>Fri, 02 Jan 2009 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">2082816</guid>        </item>
        <item>
            <title>A Novel Echocardiographic Marker of End-Systole in the Ischemic Left Ventricle - &quot;Tug of War&quot; Sign.</title>
            <link>http://www.medworm.com/index.php?rid=2082815&amp;cid=s_29164_7_f&amp;fid=29164&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19122168%26dopt%3DAbstract</link>
            <description>Conclusions: In the ischemic borderzone, SIP and VPS identified global ES with high accuracy. The force balance or &quot;tug of war&quot; between borderzone- and nonischemic myocardium is a likely underlying mechanism for these markers. The method may be used as an &quot;all in one heart beat&quot; approach for TDI analysis in acute myocardial ischemia. Key words: echocardiography, reperfusion, infarction, ventricular function.
    PMID: 19122168 [PubMed - as supplied by publisher] (Source: Am J Physiol Heart C...)</description>
            <author>Am J Physiol Heart C...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2082815</comments>
            <pubDate>Fri, 02 Jan 2009 05:00:00 +0100</pubDate>
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        <item>
            <title>Letter to the editor: &quot;Zinc and cardioprotection: the missing link&quot;.</title>
            <link>http://www.medworm.com/index.php?rid=2070235&amp;cid=s_29164_7_f&amp;fid=29164&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19116335%26dopt%3DAbstract</link>
            <description>Authors: Mocanu MM, Yellon DM
    
    PMID: 19116335 [PubMed - in process] (Source: Am J Physiol Heart C...)</description>
            <author>Am J Physiol Heart C...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2070235</comments>
            <pubDate>Thu, 01 Jan 2009 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">2070235</guid>        </item>
        <item>
            <title>Reply to &quot;Letter to the editor: 'Zinc and cardioprotection: the missing link'&quot;.</title>
            <link>http://www.medworm.com/index.php?rid=2070234&amp;cid=s_29164_7_f&amp;fid=29164&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19116336%26dopt%3DAbstract</link>
            <description>Authors: Chanoit G, Lee S, Xu Z
    
    PMID: 19116336 [PubMed - in process] (Source: Am J Physiol Heart C...)</description>
            <author>Am J Physiol Heart C...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2070234</comments>
            <pubDate>Thu, 01 Jan 2009 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">2070234</guid>        </item>
        <item>
            <title>Gene profiling of left ventricle eccentric hypertrophy in aortic regurgitation in rats: rationale for targeting the {beta}-adrenergic and renin-angiotensin systems.</title>
            <link>http://www.medworm.com/index.php?rid=2070240&amp;cid=s_29164_7_f&amp;fid=29164&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19112094%26dopt%3DAbstract</link>
            <description>Authors: Champetier S, Bojmehrani A, Beaudoin J, Lachance D, Plante E, Roussel E, Couet J, Arsenault M
    Aortic valve regurgitation (AR) imposes a severe volume overload to the left ventricle (LV) which results in dilation, eccentric hypertrophy and eventually loss of function. Little is known about the impact of AR on LV gene expression. We therefore conducted a gene expression profiling study in the LV of rats with acute and severe AR. We identified 64 genes that were specifically up-regulated and 29 that were down-regulated out of 21910 genes after 2 weeks. Of the up-regulated genes, a good proportion was related to the extracellular matrix. We subsequently studied a subset of 19 genes by quantitative RT-PCR (qRT-PCR) to see if the modulation seen in the LV after two weeks persisted i...</description>
            <author>Am J Physiol Heart C...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2070240</comments>
            <pubDate>Fri, 26 Dec 2008 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">2070240</guid>        </item>
        <item>
            <title>Cd40/cd40l contributes to hypercholesterolemia-induced microvascular inflammation.</title>
            <link>http://www.medworm.com/index.php?rid=2070239&amp;cid=s_29164_7_f&amp;fid=29164&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19112095%26dopt%3DAbstract</link>
            <description>The objective of this study was to determine whether CD40/CD40L, in particular T-cell CD40L, contributes to microvascular dysfunction induced by hypercholesterolemia. Intravital microscopy was used to quantify blood cell adhesion in cremasteric postcapillary venules, endothelium-dependent vasodilation responses in arterioles, and microvascular oxidative stress in wild-type (WT) C57Bl/6 mice, CD40-deficient ((-/-)), CD40L(-/-) or lymphocyte-deficient (SCID) mice placed on a normal (ND) or high-cholesterol (HC) diet for 2 wks. WT-HC mice exhibited an exaggerated leukocyte and platelet recruitment in venules, and impaired vasodilation responses in arterioles when compared to ND counterparts. Deficiency of CD40, CD40L or lymphocytes attenuated these responses to HC. The HC phenotype was rescue...</description>
            <author>Am J Physiol Heart C...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2070239</comments>
            <pubDate>Fri, 26 Dec 2008 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">2070239</guid>        </item>
        <item>
            <title>Chronic hypoxia enhances 15-lipoxygenase mediated vasorelaxation in rabbit arteries.</title>
            <link>http://www.medworm.com/index.php?rid=2070238&amp;cid=s_29164_7_f&amp;fid=29164&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19112096%26dopt%3DAbstract</link>
            <description>Authors: Aggarwal NT, Pfister SL, Gauthier KM, Chawengsub Y, Baker JE, Campbell WB
    15-Lipoxygenase (15-LO-1) metabolizes arachidonic acid (AA) to 11,12,15-trihydroxyeicosatrienoic acids (THETA) and 15-hydroxy-11,12-epoxyeicosatrienoic acids (HEETA) that dilate rabbit arteries. Increased endothelial 15-LO-1 expression enhances arterial relaxations to agonist. We tested the effect of hypoxia on 15-LO-1 expression, THETA and HEETA synthesis, and relaxations in the rabbit arteries. Incubation of rabbit aortic endothelial cells and isolated aortas in 0.7 % O2 increased 15-LO-1 expression. Rabbits were housed in a hypoxic atmosphere of 12 % O2 for 5 days. 15-LO-1 expression increased in the endothelium of the arteries of rabbits in 12% O2 compared to room air. THETA and HEETA synthesis was a...</description>
            <author>Am J Physiol Heart C...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2070238</comments>
            <pubDate>Fri, 26 Dec 2008 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">2070238</guid>        </item>
        <item>
            <title>Electrical remodeling in a transgenic mouse model of {alpha}1{beta}-adrenergic receptor overexpression.</title>
            <link>http://www.medworm.com/index.php?rid=2070237&amp;cid=s_29164_7_f&amp;fid=29164&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19112097%26dopt%3DAbstract</link>
            <description>Authors: Rivard K, Tr&amp;#xE9;panier-Boulay V, Rindt H, Fiset C
    Cardiac-specific overexpression of wild-type alpha1B-adrenergic receptors (alpha1beta-AR) in mice predisposes to dilated cardiomyopathy and sudden death. Although alpha-adrenergic stimulation is thought to contribute to induction of arrhythmias in heart failure, the electrophysiological consequences of chronic alpha1-adrenergic activation have not been clearly defined. Thus, we characterized ventricular repolarization and monitored incidence of spontaneous arrhythmias in end-stage heart failure alpha1beta-AR mice (9-12 months) and younger alpha1beta-AR mice (2-3 months) that do not present signs of heart failure. ECG recordings revealed that older alpha1beta-AR mice exhibited spontaneous ventricular arrhythmias. Compared to a...</description>
            <author>Am J Physiol Heart C...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2070237</comments>
            <pubDate>Fri, 26 Dec 2008 05:00:00 +0100</pubDate>
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