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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>Wed, 08 Feb 2012 09:32:26 +0100</lastBuildDate>
        <item>
            <title>CaMKII Inhibition in Heart Failure, Beneficial, Harmful or Both.</title>
            <link>http://www.medworm.com/index.php?rid=5661193&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%3D22287581%26dopt%3DAbstract</link>
            <description>Conclusions: CaMKIIδ KO cannot suppress severe pressure-overload-induced HF. Although cellular contractility is improved, it reduces in vivo cardiac reserve to β-adrenergic regulation and deteriorates diastolic function. Our findings challenge the strategy of CaMKII inhibition in HF.
    PMID: 22287581 [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=5661193</comments>
            <pubDate>Fri, 27 Jan 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5661193</guid>        </item>
        <item>
            <title>The Roles of O-linked β-N-acetylglucosamines (o-GlcNAc) in Cardiovascular Physiology and Disease.</title>
            <link>http://www.medworm.com/index.php?rid=5661192&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%3D22287582%26dopt%3DAbstract</link>
            <description>Authors: Zachara NE
    Abstract
    More than 1000 proteins of the nucleus, cytoplasm, and mitochondria are dynamically modified by O-linked β-N-acetylglucosamine (O-GlcNAc), an essential post-translational modification of metazoans. O-GlcNAc, which modifies Ser/Thr residues, is thought to regulate protein function in a manner analogous to protein phosphorylation and on a subset of proteins appears to have a reciprocal relationship with phosphorylation. Like phosphorylation, O-GlcNAc levels change dynamically in response to numerous signals including hyperglycemia and cellular injury. Recent data suggests that O-GlcNAc appears to be a key regulator of the cellular stress response, augmentation of which is protective in models of acute vascular injury, trauma hemorrhage and ischemia reper...</description>
            <author>Am J Physiol Heart C...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5661192</comments>
            <pubDate>Fri, 27 Jan 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5661192</guid>        </item>
        <item>
            <title>ALTERED SINO-ATRIAL NODE FUNCTION AND INTRA-ATRIAL CONDUCTION IN MURINE GAIN-OF-FUNCTION Scn5a+/{Delta}KPQ HEARTS SUGGEST AN OVERLAP SYNDROME.</title>
            <link>http://www.medworm.com/index.php?rid=5661190&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%3D22287583%26dopt%3DAbstract</link>
            <description>Conclusions:&amp;lt;/BOLD&amp;gt; The gain-of-function LQT3 murine Scn5a+/ΔKPQ cardiac system, in overlap with corresponding features reported in loss-of-function Na(+) channel mutations, shows compromised SAN pacemaker and conduction function explicable in modeling studies through a combination of augmented tail and reduced peak Na(+) currents.
    PMID: 22287583 [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=5661190</comments>
            <pubDate>Fri, 27 Jan 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5661190</guid>        </item>
        <item>
            <title>Pressure-Overload Dependent Membrane-Type 1 Matrix Metalloproteinase Induction: Relationship to LV Remodeling and Fibrosis.</title>
            <link>http://www.medworm.com/index.php?rid=5661189&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%3D22287584%26dopt%3DAbstract</link>
            <description>Conclusions: These findings challenge the canonical belief that PO suppresses overall matrix proteolytic activity, but rather supports the concept that certain proteases, such as MT1-MMP, play a pivotal role in pressure-overload induced matrix remodeling and fibrosis.
    PMID: 22287584 [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=5661189</comments>
            <pubDate>Fri, 27 Jan 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5661189</guid>        </item>
        <item>
            <title>Effect of heart rate on hemodynamic endpoints under concomitant microvascular disease in a porcine model.</title>
            <link>http://www.medworm.com/index.php?rid=5661188&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%3D22287585%26dopt%3DAbstract</link>
            <description>Conclusion. Under MVD conditions, FFR, CDP, and LFC were not significantly influenced by changes in HR while they can significantly distinguish %AS and DP groups.
    PMID: 22287585 [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=5661188</comments>
            <pubDate>Fri, 27 Jan 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5661188</guid>        </item>
        <item>
            <title>The onset of left ventricular diastolic dysfunction in SHR rats is not related to hypertrophy or hypertension.</title>
            <link>http://www.medworm.com/index.php?rid=5661187&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%3D22287586%26dopt%3DAbstract</link>
            <description>Authors: Dupont S, Maizel J, Mentaverri R, Chillon JM, Six I, Giummelly P, Brazier M, Choukroun G, Tribouilloy C, Massy ZA, Slama M
    Abstract
    Left ventricular (LV) diastolic dysfunction, particularly relaxation abnormalities, are known to be associated with the development of left ventricular hypertrophy (LVH). Preliminary human and animal studies suggested that early LV diastolic dysfunction may be revealed independently of LVH. However, whether LV diastolic dysfunction is compromised before the onset of hypertension and LVH remains unknown. We therefore evaluated LV diastolic function in spontaneously hypertensive rats (SHR) at different ages and tested whether LV diastolic dysfunction is associated with abnormal intracellular calcium homeostasis. LV systolic and diastolic functio...</description>
            <author>Am J Physiol Heart C...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5661187</comments>
            <pubDate>Fri, 27 Jan 2012 05:00:00 +0100</pubDate>
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            <title>Sympathetic Activation and Nitric Oxide Function in Early Hypertension.</title>
            <link>http://www.medworm.com/index.php?rid=5661186&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%3D22287587%26dopt%3DAbstract</link>
            <description>Conclusions: Our results suggest that sympathetic activity plays a role in hypertension. NO tonically restrains blood pressure by ~30 mmHg, but we found no evidence of impaired modulation by NO of vascular tone contributing to the early development of hypertension. If NO deficiency contributes to hypertension, it is likely to be due through interactions with the autonomic nervous system, which were excluded in this study.
    PMID: 22287587 [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=5661186</comments>
            <pubDate>Fri, 27 Jan 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5661186</guid>        </item>
        <item>
            <title>Am J Physiol Heart Circ Physiol; +54 new citations</title>
            <link>http://www.medworm.com/index.php?rid=5625577&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%25222012%252F01%252F12%252011.42%2522%255BMHDA%255D%253A%25222012%252F01%252F25%252002.29%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%25222012%252F01%252F12%252011.42%2522%255BEDAT%255D%29%29</link>
            <description>54 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 2012/01/25PubMed, 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=5625577</comments>
            <pubDate>Wed, 25 Jan 2012 07:29:59 +0100</pubDate>
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        <item>
            <title>Wave Intensity Analysis of Para-aortic Counterpulsation.</title>
            <link>http://www.medworm.com/index.php?rid=5579638&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%3D22227124%26dopt%3DAbstract</link>
            <description>Authors: Lu PJ, Yang CF, Wu MY, Hung CH, Chan MY, Hsu TC
    Abstract
    A novel wave intensity analysis (WIA) was used to delineate and maximize the efficacy of a newly developed para-aortic blood pump (PABP). The gold-standard intra-aortic balloon pump (IABP) was employed as the comparison benchmark. Acute porcine experiments using 8 pigs, randomly divided into IABP (n=4) and PABP (n=4) groups, were conducted to compare the characteristics of intra- and para-aortic counterpulsation. We measured pressure and velocity with probes installed in the left anterior descending (LAD) coronary artery and aorta, during and without PABP assistance. Wave intensity for aortic and left coronary waves were derived from pressure and flow measurements with synchronization correction applied. To achieve m...</description>
            <author>Am J Physiol Heart C...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5579638</comments>
            <pubDate>Fri, 06 Jan 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5579638</guid>        </item>
        <item>
            <title>The cannabinoid receptor CB2 protects against balloon-induced neointima formation.</title>
            <link>http://www.medworm.com/index.php?rid=5579637&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%3D22227125%26dopt%3DAbstract</link>
            <description>In conclusion, pharmacological activation or genetic deletion of CB(2) receptors modulate neointima formation via protective effects in macrophages and smooth muscle cells.
    PMID: 22227125 [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=5579637</comments>
            <pubDate>Fri, 06 Jan 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5579637</guid>        </item>
        <item>
            <title>The Renin Angiotensin System: A Target of and Contributor to Dyslipidemias, Altered Glucose Homeostasis and Hypertension of the Metabolic Syndrome.</title>
            <link>http://www.medworm.com/index.php?rid=5579636&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%3D22227126%26dopt%3DAbstract</link>
            <description>Authors: Putnam K, Shoemaker R, Yiannikouris F, Cassis LA
    Abstract
    The renin-angiotensin system (RAS) is an important therapeutic target in the treatment of hypertension. Obesity has emerged as a primary contributor to essential hypertension in the US, and clusters with other metabolic disorders (hyperglycemia, hypertension, high triglycerides, low HDL cholesterol) defined within the metabolic syndrome. In addition to hypertension, RAS blockade may also serve as an effective treatment strategy to control impaired glucose and insulin tolerance and dyslipidemias in patients with the metabolic syndrome. Hyperglycemia, insulin resistance, and/or specific cholesterol metabolites have been demonstrated to activate components required for the synthesis (angiotensinogen, renin, ACE), degra...</description>
            <author>Am J Physiol Heart C...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5579636</comments>
            <pubDate>Fri, 06 Jan 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5579636</guid>        </item>
        <item>
            <title>Intermedin elicits a negative inotropic effect in rat papillary muscles mediated by endothelial derived nitric oxide.</title>
            <link>http://www.medworm.com/index.php?rid=5579635&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%3D22227127%26dopt%3DAbstract</link>
            <description>Authors: Pires AL, Pinho M, Sena CM, Seiça RM, Leite-Moreira AF
    Abstract
    Intermedin (IMD) is a novel vasoactive peptide from the calcitonin gene-related peptide (CGRP) implicated in cardiac regulation, yet the contractile effects of IMD remain controversial, since previous studies in vivo and isolated cardiomyocytes documented contradictory results. We hypothesized cardiac endothelial cells involvement in IMD modulation of cardiac function as an explanation for these opposing observations. With this in mind, we investigated the direct action of increasing concentrations of IMD (10(-8) to 10(-6)M) on myocardial performance parameters in rat left ventricular (LV) papillary muscles with and without endocardial endothelium (EE) and in presence of receptor antagonists and intracellular...</description>
            <author>Am J Physiol Heart C...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5579635</comments>
            <pubDate>Fri, 06 Jan 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5579635</guid>        </item>
        <item>
            <title>G Protein Mediated Stretch Reception.</title>
            <link>http://www.medworm.com/index.php?rid=5579634&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%3D22227128%26dopt%3DAbstract</link>
            <description>Authors: Storch U, Mederos Y Schnitzler M, Gudermann T
    Abstract
    Mechanosensation and -transduction are important for physiological processes like the senses of touch, hearing and balance. The mechanisms underlying the translation of mechanical stimuli into biochemical information by activating various signaling pathways play a fundamental role in physiology and pathophysiology, but are only poorly understood. Recently, G protein-coupled receptors (GPCRs), which are essential for the conversion of light, olfactory and gustatory stimuli as well as of primary messengers like hormones and neurotransmitters into cellular signals and play distinct roles in inflammation, cell growth and differentiation, have emerged as potential mechanosensors. The first candidate for a mechanosensitive G...</description>
            <author>Am J Physiol Heart C...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5579634</comments>
            <pubDate>Fri, 06 Jan 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5579634</guid>        </item>
        <item>
            <title>Sympathetic activation increases basilar arterial blood flow in normotensive but not hypertensive rats.</title>
            <link>http://www.medworm.com/index.php?rid=5564785&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%3D22210747%26dopt%3DAbstract</link>
            <description>Authors: Chang HH, Lee YC, Chen MF, Kuo JS, Lee TJ
    Abstract
    The close apposition between sympathetic and parasympathetic nerve terminals in the adventitia of cerebral arteries provides morphological evidence that sympathetic nerve activation causes parasympathetic nitrergic vasodilation via sympathetic-parasympathetic-interaction mechanism. The decreased parasympathetic nerve terminals in basilar arteries (BA) of spontaneously hypertensive rat (SHR) and renovascular hypertensive rats (RHR) comparing to Wistar-Kyoto rats (WKY), therefore, would diminish this axo-axonal-interaction-mediated neurogenic vasodilation in hypertension. Increased basilar arterial blood flow (BABF) via axo-axonal interaction during sympathetic activation was, therefore, examined in anesthetized rats by lase...</description>
            <author>Am J Physiol Heart C...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5564785</comments>
            <pubDate>Fri, 30 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5564785</guid>        </item>
        <item>
            <title>Spatio-temporal attributes of left ventricular pressure decay rate during isovolumic relaxation.</title>
            <link>http://www.medworm.com/index.php?rid=5564784&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%3D22210748%26dopt%3DAbstract</link>
            <description>Authors: Ghosh E, Kovács SJ
    Abstract
    Global left ventricular (LV) isovolumic relaxation rate has been characterized: 1) via the time-constant of isovolumic relaxation τ or 2) via the logistic time-constant τ(L). An alternate kinematic method, characterizes isovolumic relaxation (IVR) in accordance with Newton's Second Law. The model's parameters - stiffness E(k), and damping/relaxation μ result from best fit of model-predicted pressure to in-vivo data. All three models (exponential, logistic and kinematic) characterize global relaxation in terms of pressure decay rates. However, IVR is inhomogeneous and anisotropic. Apical and basal wall segments untwist at different times and rates, transmural strain and strain-rates differ due to the helically variable pitch of myocytes and s...</description>
            <author>Am J Physiol Heart C...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5564784</comments>
            <pubDate>Fri, 30 Dec 2011 05:00:00 +0100</pubDate>
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        <item>
            <title>Adiponectin and adipocyte fatty acid binding protein in the pathogenesis of cardiovascular disease.</title>
            <link>http://www.medworm.com/index.php?rid=5564783&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%3D22210749%26dopt%3DAbstract</link>
            <description>Authors: Xu A, Vanhoutte PM
    Abstract
    The heart and blood vessels are surrounded by epicardial and perivascular adipose tissues respectively, which play important roles in maintaining cardiovascular homeostasis by secreting a number of biologically active molecules, termed &quot;adipokines&quot;. Many of these adipokines function as an important component of the 'adipo-cardiovascular axis' mediating the cross-talk between adipose tissues, the heart, and the vasculature. On the one hand, most adipokines [including tumor necrosis factor α, resistin, adipocyte fatty acid binding protein (A-FABP) and lipocalin-2] are pro-inflammatory and causally associated with endothelial and cardiac dysfunction by their endocrine/paracrine actions. On the other hand, adiponectin is one of the few adipokines t...</description>
            <author>Am J Physiol Heart C...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5564783</comments>
            <pubDate>Fri, 30 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5564783</guid>        </item>
        <item>
            <title>Right ventricular regional wall curvedness and area strain in patients with repaired Tetralogy of Fallot.</title>
            <link>http://www.medworm.com/index.php?rid=5564782&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%3D22210750%26dopt%3DAbstract</link>
            <description>The objective of this study is to quantify the regional curvatures and area strain (AS) based on three-dimensional (3D) reconstructions of the RV using cardiac magnetic resonance imaging (MRI). Fourteen (14) rTOF patients and nine (9) normal subjects underwent cardiac MRI scan. 3D RV endocardial surface models were reconstructed from manually delineated contours and correspondence between end-diastole (ED) and end-systole (ES) was determined. Regional curvedness (C) and surface area at end-diastole and end-systole were calculated as well as the area strain. The RV shape and deformation in rTOF patients differed from normal subjects in several respects. Firstly, the curvedness at ED (mean for 13 segments, 0.030±0.0076 mm(-1) vs. 0.029±0.0065 mm(-1) , p &amp;lt; 0.05) and ES (mean for 13 segme...</description>
            <author>Am J Physiol Heart C...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5564782</comments>
            <pubDate>Fri, 30 Dec 2011 05:00:00 +0100</pubDate>
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        <item>
            <title>Angiotensin II-induced reduction in exercise capacity is associated with increased oxidative stress in skeletal muscle.</title>
            <link>http://www.medworm.com/index.php?rid=5564781&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%3D22210751%26dopt%3DAbstract</link>
            <description>Authors: Inoue N, Kinugawa S, Suga T, Yokota T, Hirabayashi K, Kuroda S, Okita K, Tsutsui H
    Abstract
    Angiotensin II (Ang II)-induced oxidative stress has been known to be involved in the pathogenesis of cardiovascular diseases. We have reported that the oxidative stress in skeletal muscle can limit exercise capacity in mice. We thus hypothesized that Ang II could impair the skeletal muscle energy metabolism and limit exercise capacity via enhancing oxidative stress. Ang II (50 ng/kg/min) or vehicle was infused into male C57BL/6J mice for 7 days via subcutaneously implanted osmotic minipumps. Ang II did not alter body weight, skeletal muscle weight, blood pressure, cardiac structure and function. Mice were treadmill-tested and expired gases were analyzed. The work to exhaustion (ver...</description>
            <author>Am J Physiol Heart C...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5564781</comments>
            <pubDate>Fri, 30 Dec 2011 05:00:00 +0100</pubDate>
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        <item>
            <title>Am J Physiol Heart Circ Physiol; +53 new citations</title>
            <link>http://www.medworm.com/index.php?rid=5537109&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%25222011%252F12%252F18%252019.36%2522%255BMHDA%255D%253A%25222011%252F12%252F24%252017.24%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%25222011%252F12%252F18%252019.36%2522%255BEDAT%255D%29%29</link>
            <description>53 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 2011/12/24PubMed, 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>
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            <pubDate>Sat, 24 Dec 2011 22:24:01 +0100</pubDate>
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            <title>Am J Physiol Heart Circ Physiol; +90 new citations</title>
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            <description>90 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 2011/12/18PubMed, 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>
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            <pubDate>Mon, 19 Dec 2011 00:36:01 +0100</pubDate>
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            <title>Am J Physiol Heart Circ Physiol; +28 new citations</title>
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            <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 2011/11/19PubMed, 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>
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            <pubDate>Sat, 19 Nov 2011 22:06:03 +0100</pubDate>
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            <title>Am J Physiol Heart Circ Physiol; +73 new citations</title>
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            <description>73 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 2011/11/07PubMed, 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>
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            <title>Am J Physiol Heart Circ Physiol; +29 new citations</title>
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            <description>29 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 2011/10/25PubMed, 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>
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            <pubDate>Wed, 26 Oct 2011 01:44:54 +0100</pubDate>
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            <title>Am J Physiol Heart Circ Physiol; +112 new citations</title>
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            <description>112 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 2011/10/04PubMed, 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>
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        <comments>http://www.medworm.com/rss/comments.php?id=5282869</comments>
            <pubDate>Wed, 05 Oct 2011 02:34:54 +0100</pubDate>
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            <title>Am J Physiol Heart Circ Physiol; +37 new citations</title>
            <link>http://www.medworm.com/index.php?rid=5179883&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%25222011%252F08%252F26%252014.12%2522%255BMHDA%255D%253A%25222011%252F09%252F01%252012.16%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%25222011%252F08%252F26%252014.12%2522%255BEDAT%255D%29%29</link>
            <description>37 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 2011/09/01PubMed, 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=5179883</comments>
            <pubDate>Thu, 01 Sep 2011 16:16:02 +0100</pubDate>
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            <title>Am J Physiol Heart Circ Physiol; +65 new citations</title>
            <link>http://www.medworm.com/index.php?rid=5160061&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%25222011%252F08%252F20%252003.30%2522%255BMHDA%255D%253A%25222011%252F08%252F26%252014.12%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%25222011%252F08%252F20%252003.30%2522%255BEDAT%255D%29%29</link>
            <description>65 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 2011/08/26PubMed, 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=5160061</comments>
            <pubDate>Fri, 26 Aug 2011 18:12:02 +0100</pubDate>
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        <item>
            <title>Am J Physiol Heart Circ Physiol; +16 new citations</title>
            <link>http://www.medworm.com/index.php?rid=5108178&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%25222011%252F07%252F26%252011.45%2522%255BMHDA%255D%253A%25222011%252F08%252F09%252018.30%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%25222011%252F07%252F26%252011.45%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 2011/08/09PubMed, 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=5108178</comments>
            <pubDate>Tue, 09 Aug 2011 22:30:02 +0100</pubDate>
            <guid isPermaLink="false">5108178</guid>        </item>
        <item>
            <title>Am J Physiol Heart Circ Physiol; +18 new citations</title>
            <link>http://www.medworm.com/index.php?rid=5063580&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%25222011%252F07%252F11%252020.15%2522%255BMHDA%255D%253A%25222011%252F07%252F26%252011.45%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%25222011%252F07%252F11%252020.15%2522%255BEDAT%255D%29%29</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 2011/07/26PubMed, 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=5063580</comments>
            <pubDate>Tue, 26 Jul 2011 15:45:02 +0100</pubDate>
            <guid isPermaLink="false">5063580</guid>        </item>
        <item>
            <title>Am J Physiol Heart Circ Physiol; +63 new citations</title>
            <link>http://www.medworm.com/index.php?rid=5011812&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%25222011%252F06%252F26%252015.00%2522%255BMHDA%255D%253A%25222011%252F07%252F11%252020.15%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%25222011%252F06%252F26%252015.00%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 2011/07/11PubMed, 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=5011812</comments>
            <pubDate>Tue, 12 Jul 2011 00:15:02 +0100</pubDate>
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        <item>
            <title>Am J Physiol Heart Circ Physiol; +75 new citations</title>
            <link>http://www.medworm.com/index.php?rid=4968094&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%25222011%252F06%252F12%252006.30%2522%255BMHDA%255D%253A%25222011%252F06%252F26%252015.00%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%25222011%252F06%252F12%252006.30%2522%255BEDAT%255D%29%29</link>
            <description>75 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 2011/06/26PubMed, 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=4968094</comments>
            <pubDate>Sun, 26 Jun 2011 19:00:03 +0100</pubDate>
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        <item>
            <title>Am J Physiol Heart Circ Physiol; +25 new citations</title>
            <link>http://www.medworm.com/index.php?rid=4922175&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%25222011%252F05%252F29%252002.30%2522%255BMHDA%255D%253A%25222011%252F06%252F12%252006.30%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%25222011%252F05%252F29%252002.30%2522%255BEDAT%255D%29%29</link>
            <description>25 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 2011/06/12PubMed, 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=4922175</comments>
            <pubDate>Sun, 12 Jun 2011 10:30:02 +0100</pubDate>
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        <item>
            <title>Am J Physiol Heart Circ Physiol; +74 new citations</title>
            <link>http://www.medworm.com/index.php?rid=4876204&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%25222011%252F05%252F14%252013.45%2522%255BMHDA%255D%253A%25222011%252F05%252F29%252002.30%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%25222011%252F05%252F14%252013.45%2522%255BEDAT%255D%29%29</link>
            <description>74 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 2011/05/29PubMed, 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=4876204</comments>
            <pubDate>Sun, 29 May 2011 06:30:03 +0100</pubDate>
            <guid isPermaLink="false">4876204</guid>        </item>
        <item>
            <title>Am J Physiol Heart Circ Physiol; +20 new citations</title>
            <link>http://www.medworm.com/index.php?rid=4822046&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%25222011%252F04%252F30%252013.00%2522%255BMHDA%255D%253A%25222011%252F05%252F14%252013.45%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%25222011%252F04%252F30%252013.00%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 2011/05/14PubMed, 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=4822046</comments>
            <pubDate>Sat, 14 May 2011 17:45:02 +0100</pubDate>
            <guid isPermaLink="false">4822046</guid>        </item>
        <item>
            <title>Exercise-mediated changes in conduit artery wall thickness in humans: role of shear stress.</title>
            <link>http://www.medworm.com/index.php?rid=4768407&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%3D21515668%26dopt%3DAbstract</link>
            <description>EXERCISE-MEDIATED CHANGES IN CONDUIT ARTERY WALL THICKNESS IN HUMANS: ROLE OF SHEAR STRESS.
    Am J Physiol Heart Circ Physiol. 2011 Apr 22;
    Authors: Thijssen DH, Dawson EA, van de Munckhof I, Tinken TM, Den Drijver E, Hopkins N, Cable NT, Green DJ
    Episodic increases in shear stress have been proposed as a mechanism which induces training-induced adaptation in arterial wall remodeling in humans. To address this hypothesis in humans, we examined bilateral brachial artery wall thickness using high-resolution ultrasound in healthy men across an 8-week period of bilateral handgrip training. Unilaterally, shear rate was attenuated by cuff inflation to 60 mmHg. Grip strength, forearm volume and girth improved similarly between the limbs. Acute bouts of handgrip exercise increased shear ...</description>
            <author>Am J Physiol Heart C...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4768407</comments>
            <pubDate>Thu, 21 Apr 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4768407</guid>        </item>
        <item>
            <title>Adiponectin opposes endothelin-1-mediated vasoconstriction in the perfused rat hindlimb.</title>
            <link>http://www.medworm.com/index.php?rid=4768406&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%3D21515669%26dopt%3DAbstract</link>
            <description>Authors: Bussey CT, Kolka CM, Rattigan S, Richards SM
    Recent studies have shown that adiponectin is able to increase nitric oxide (NO) production by the endothelium and relax pre-constricted isolated aortic rings, suggesting that adiponectin may act as a vasodilator. Endothelin-1 (ET-1) is a potent vasoconstrictor, elevated levels of which are associated with obesity, type 2 diabetes, hypertension and cardiovascular disease. We hypothesised that adiponectin has NO-dependent vascular actions opposing the vasoconstrictor actions of ET-1. We studied the vascular and metabolic effects of a physiological concentration of adiponectin (6.5μg.mL(-1)) on Hooded Wistar rats in the constant-flow pump-perfused rat hindlimb. Adiponectin alone had no observable vascular activity; however, adiponect...</description>
            <author>Am J Physiol Heart C...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4768406</comments>
            <pubDate>Thu, 21 Apr 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4768406</guid>        </item>
        <item>
            <title>Am J Physiol Heart Circ Physiol; +20 new citations</title>
            <link>http://www.medworm.com/index.php?rid=4716487&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%25222011%252F03%252F31%252022.45%2522%255BMHDA%255D%253A%25222011%252F04%252F15%252017.30%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%25222011%252F03%252F31%252022.45%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 2011/04/15PubMed, 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=4716487</comments>
            <pubDate>Fri, 15 Apr 2011 21:30:02 +0100</pubDate>
            <guid isPermaLink="false">4716487</guid>        </item>
        <item>
            <title>Am J Physiol Heart Circ Physiol; +19 new citations</title>
            <link>http://www.medworm.com/index.php?rid=4662236&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%25222011%252F03%252F17%252011.00%2522%255BMHDA%255D%253A%25222011%252F03%252F31%252022.45%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%25222011%252F03%252F17%252011.00%2522%255BEDAT%255D%29%29</link>
            <description>19 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 2011/03/31PubMed, 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=4662236</comments>
            <pubDate>Fri, 01 Apr 2011 02:45:02 +0100</pubDate>
            <guid isPermaLink="false">4662236</guid>        </item>
        <item>
            <title>Am J Physiol Heart Circ Physiol; +51 new citations</title>
            <link>http://www.medworm.com/index.php?rid=4601182&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%25222011%252F03%252F03%252003.45%2522%255BMHDA%255D%253A%25222011%252F03%252F17%252011.00%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%25222011%252F03%252F03%252003.45%2522%255BEDAT%255D%29%29</link>
            <description>51 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 2011/03/17PubMed, 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=4601182</comments>
            <pubDate>Thu, 17 Mar 2011 15:00:03 +0100</pubDate>
            <guid isPermaLink="false">4601182</guid>        </item>
        <item>
            <title>Am J Physiol Heart Circ Physiol; +30 new citations</title>
            <link>http://www.medworm.com/index.php?rid=4540792&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%25222011%252F02%252F17%252002.15%2522%255BMHDA%255D%253A%25222011%252F03%252F03%252003.45%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%25222011%252F02%252F17%252002.15%2522%255BEDAT%255D%29%29</link>
            <description>30 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 2011/03/03PubMed, 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=4540792</comments>
            <pubDate>Thu, 03 Mar 2011 08:45:03 +0100</pubDate>
            <guid isPermaLink="false">4540792</guid>        </item>
        <item>
            <title>Am J Physiol Heart Circ Physiol; +73 new citations</title>
            <link>http://www.medworm.com/index.php?rid=4483635&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%25222011%252F01%252F31%252006.00%2522%255BMHDA%255D%253A%25222011%252F02%252F17%252002.15%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%25222011%252F01%252F31%252006.00%2522%255BEDAT%255D%29%29</link>
            <description>73 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 2011/02/17PubMed, 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=4483635</comments>
            <pubDate>Thu, 17 Feb 2011 07:15:03 +0100</pubDate>
            <guid isPermaLink="false">4483635</guid>        </item>
        <item>
            <title>Am J Physiol Heart Circ Physiol; +24 new citations</title>
            <link>http://www.medworm.com/index.php?rid=4415091&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%25222011%252F01%252F16%252012.45%2522%255BMHDA%255D%253A%25222011%252F01%252F31%252006.00%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%25222011%252F01%252F16%252012.45%2522%255BEDAT%255D%29%29</link>
            <description>24 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 2011/01/31PubMed, 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=4415091</comments>
            <pubDate>Mon, 31 Jan 2011 11:00:03 +0100</pubDate>
            <guid isPermaLink="false">4415091</guid>        </item>
        <item>
            <title>Am J Physiol Heart Circ Physiol; +75 new citations</title>
            <link>http://www.medworm.com/index.php?rid=4353453&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%252F12%252F24%252001.10%2522%255BMHDA%255D%253A%25222011%252F01%252F16%252012.45%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%252F12%252F24%252001.10%2522%255BEDAT%255D%29%29</link>
            <description>75 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 2011/01/16PubMed, 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=4353453</comments>
            <pubDate>Sun, 16 Jan 2011 17:45:02 +0100</pubDate>
            <guid isPermaLink="false">4353453</guid>        </item>
        <item>
            <title>Am J Physiol Heart Circ Physiol; +21 new citations</title>
            <link>http://www.medworm.com/index.php?rid=4285378&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%252F12%252F14%252011.40%2522%255BMHDA%255D%253A%25222010%252F12%252F24%252001.10%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%252F12%252F14%252011.40%2522%255BEDAT%255D%29%29</link>
            <description>21 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 2010/12/24PubMed, 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=4285378</comments>
            <pubDate>Fri, 24 Dec 2010 06:10:02 +0100</pubDate>
            <guid isPermaLink="false">4285378</guid>        </item>
        <item>
            <title>Am J Physiol Heart Circ Physiol; +100 new citations</title>
            <link>http://www.medworm.com/index.php?rid=4256880&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%252F12%252F03%252004.25%2522%255BMHDA%255D%253A%25222010%252F12%252F14%252011.40%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%252F12%252F03%252004.25%2522%255BEDAT%255D%29%29</link>
            <description>100 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 2010/12/14PubMed, 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=4256880</comments>
            <pubDate>Tue, 14 Dec 2010 16:40:11 +0100</pubDate>
            <guid isPermaLink="false">4256880</guid>        </item>
        <item>
            <title>Spatial and temporal heterogeneities are localized to the right ventricular outflow tract in a heterozygotic Scn5a mouse model.</title>
            <link>http://www.medworm.com/index.php?rid=4204670&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%3D21097662%26dopt%3DAbstract</link>
            <description>Authors: Martin CA, Grace AA, Huang CL
    Ventricular tachycardia (VT) in Brugada Syndrome (BrS) patients often originates in the right ventricular outflow tract (RVOT). We explore the physiological basis for this observation using murine whole-heart preparations. Ventricular bipolar electrograms and monophasic action potentials were recorded from 7 epicardial positions in Langendorff-perfused WT and Scn5a(+/-) hearts. VT first appeared in the RVOT, implicating it as an arrhythmogenic focus in Scn5a(+/-) hearts. RVOTs showed the greatest heterogeneity in refractory periods, activation latencies and action potential (AP) durations, and the most fractionated electrograms. However, incidences of concordant alternans in dynamic pacing protocol recordings were unaffected by the Scn5a(+/-) muta...</description>
            <author>Am J Physiol Heart C...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4204670</comments>
            <pubDate>Fri, 19 Nov 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4204670</guid>        </item>
        <item>
            <title>Slow and incomplete sympathetic reinnervation of rat tail artery restores the amplitude of nerve-evoked contractions provided a perivascular plexus is present.</title>
            <link>http://www.medworm.com/index.php?rid=4204669&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%3D21097663%26dopt%3DAbstract</link>
            <description>Authors: Tripovic D, Pianova S, McLachlan EM, Brock JA
    We have investigated the recovery of sympathetic control following reinnervation of denervated rat tail arteries by relating the reappearance of noradrenergic terminals to the amplitude of nerve-evoked contractions of isometrically mounted artery segments in vitro. We have also assessed reactivity to vasoconstrictor agonists. Freezing the collector nerves near the base of the tail in adult rats denervated the artery from ~40 mm along the tail. Restoration of the perivascular plexus declined along the length of the tail, remaining incomplete for &amp;gt;6 months. After 4 months, nerve-evoked contractions were of comparable amplitude to control at ~60 mm along the tail, but smaller at ~110 mm, and were prolonged. At ~60 mm, facilitation ...</description>
            <author>Am J Physiol Heart C...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4204669</comments>
            <pubDate>Fri, 19 Nov 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4204669</guid>        </item>
        <item>
            <title>Am J Physiol Heart Circ Physiol; +21 new citations</title>
            <link>http://www.medworm.com/index.php?rid=4172345&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%252F11%252F07%252011.45%2522%255BMHDA%255D%253A%25222010%252F11%252F16%252019.55%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%252F11%252F07%252011.45%2522%255BEDAT%255D%29%29</link>
            <description>21 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 2010/11/16PubMed, 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=4172345</comments>
            <pubDate>Wed, 17 Nov 2010 00:55:04 +0100</pubDate>
            <guid isPermaLink="false">4172345</guid>        </item>
        <item>
            <title>Am J Physiol Heart Circ Physiol; +85 new citations</title>
            <link>http://www.medworm.com/index.php?rid=4014420&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%252F09%252F11%252013.03%2522%255BMHDA%255D%253A%25222010%252F09%252F30%252008.55%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%252F09%252F11%252013.03%2522%255BEDAT%255D%29%29</link>
            <description>85 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 2010/09/30PubMed, 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=4014420</comments>
            <pubDate>Thu, 30 Sep 2010 12:55:02 +0100</pubDate>
            <guid isPermaLink="false">4014420</guid>        </item>
        <item>
            <title>Am J Physiol Heart Circ Physiol; +58 new citations</title>
            <link>http://www.medworm.com/index.php?rid=3958480&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%252F08%252F26%252012.42%2522%255BMHDA%255D%253A%25222010%252F09%252F11%252013.03%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%252F08%252F26%252012.42%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 2010/09/11PubMed, 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=3958480</comments>
            <pubDate>Sat, 11 Sep 2010 17:03:02 +0100</pubDate>
            <guid isPermaLink="false">3958480</guid>        </item>
        <item>
            <title>Both A2a and A2b adenosine receptors at reperfusion are necessary to reduce infarct size in mouse hearts.</title>
            <link>http://www.medworm.com/index.php?rid=3873530&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%3D20709859%26dopt%3DAbstract</link>
            <description>Authors: Methner C, Schmidt K, Cohen MV, Downey JM, Krieg T
    Pre- and postconditioning depend on activation of adenosine receptors at the end of the index ischemia. The aim of this study was to determine which receptor subtypes must be activated. In situ mouse hearts underwent 30 min of regional ischemia followed by 2 h of reperfusion. As expected, either ischemic postconditioning (six cycles of 10 sec of reperfusion and 10 sec of coronary occlusion) or infusion of the selective A(2b) adenosine receptor (A(2b)AR) agonist BAY60-6583 (BAY60) for 60 min starting 5 min prior to reperfusion reduced infarct size in wild-type C57Bl/6N mice. Protection from either was abolished by the selective A(2b)AR antagonist MRS1754 confirming a role for A(2b)AR. Additionally, co-administration of ischemic...</description>
            <author>Am J Physiol Heart C...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3873530</comments>
            <pubDate>Thu, 12 Aug 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">3873530</guid>        </item>
        <item>
            <title>Exploring the role of pH in modulating effects of lidocaine in a virtual ischemic tissue.</title>
            <link>http://www.medworm.com/index.php?rid=3873529&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%3D20709860%26dopt%3DAbstract</link>
            <description>In conclusion, the present simulation study uses the new formulated model of lidocaine, which considers pH and frequency-modulation, and sheds light into the mechanisms by which lidocaine facilitates the onset of reentries, and brings understanding also of the potential antifibrillatory effects of the drug.
    PMID: 20709860 [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=3873529</comments>
            <pubDate>Thu, 12 Aug 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">3873529</guid>        </item>
        <item>
            <title>Age-dependent cardiopulmonary interaction during airway obstruction: a simulation model.</title>
            <link>http://www.medworm.com/index.php?rid=3873528&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%3D20709861%26dopt%3DAbstract</link>
            <description>Authors: Goldman E
    Inspiratory fall in arterial blood pressure (Pa) during airway obstruction was ascribed to ventricular interdependence, afterload, and transmission of intrathoracic pressure swings. We have shown this effect significantly reduced in the elderly, but the underlying reasons remain unclear. Here we compare the results of inspiratory loading in young and older subjects with a mathematical model that simulated beat-by-beat fluctuations in cardiopulmonary variables. By increasing arterial and left ventricular elastance parameters in the older group, simulations strongly correlated with the experimental Pa and identified a linear increase of left ventricular transmural pressures with negative intrathoracic pressure that was nearly 38% larger than in the younger group. The a...</description>
            <author>Am J Physiol Heart C...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3873528</comments>
            <pubDate>Thu, 12 Aug 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">3873528</guid>        </item>
        <item>
            <title>Essential role of ER-alpha-dependent NO production in resveratrol-mediated inhibition of restenosis.</title>
            <link>http://www.medworm.com/index.php?rid=3873527&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%3D20709862%26dopt%3DAbstract</link>
            <description>Authors: Khandelwal AR, Hebert VY, Dugas TR
    Resveratrol, a red wine polyphenol, is known to exhibit vascular-protective effects and reduce vascular smooth muscle cell mitogenesis. Vascular smooth muscle cell proliferation is a critical factor in the pathogenesis of restenosis, the re-narrowing of vessels that often occurs after angioplasty and/or stent implantation. Though resveratrol has been shown to be an estrogen receptor (ER) modulator, the role of the ER in resveratrol-mediated protection against restenosis has not yet been elucidated in vivo. Therefore, using a mouse carotid artery injury model, our objective was to determine the role of ER-alpha in modulating resveratrol-mediated effects on neointimal hyperplasia. Female wild-type and estrogen receptor-alpha (-/-) mice were adm...</description>
            <author>Am J Physiol Heart C...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3873527</comments>
            <pubDate>Thu, 12 Aug 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">3873527</guid>        </item>
        <item>
            <title>Disruption of Adenylyl Cyclase Type V does not Rescue the Phenotype of Cardiac-Specific Over-Expression of G{alpha}q Protein-Induced Cardiomyopathy.</title>
            <link>http://www.medworm.com/index.php?rid=3873526&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%3D20709863%26dopt%3DAbstract</link>
            <description>In conclusion, unlike other established models of cardiomyopathy, disrupting AC(V) expression in the G(alphaq) mouse model is insufficient to overcome several parallel pathophysiological processes leading to progressive heart failure.
    PMID: 20709863 [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=3873526</comments>
            <pubDate>Thu, 12 Aug 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">3873526</guid>        </item>
        <item>
            <title>Two-photon Microscopy Guided Femtosecond-laser Photoablation of Avian Cardiogenesis: Noninvasive Creation of Localized Heart Defects.</title>
            <link>http://www.medworm.com/index.php?rid=3873525&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%3D20709864%26dopt%3DAbstract</link>
            <description>Authors: Yalcin HC, Shekhar A, Nishimura N, Rane AA, Schaffer CB, Butcher JT
    Embryonic heart formation is driven by complex feedback between genetic and hemodynamic stimuli. Clinical congenital heart defects (CHD), however, often manifest as localized micro-tissue malformations with no underlying genetic mutation - suggesting altered hemodynamics during embryonic development may play a role. Investigation of this relationship has been impaired by a lack of experimental tools that can create locally targeted cardiac perturbations. Here, we have developed noninvasive optical techniques which can modulate avian cardiogenesis to dissect relationships between alterations in mechanical signaling and CHD. We used two-photon excited fluorescence (2PEF) microscopy to monitor cushion and ventric...</description>
            <author>Am J Physiol Heart C...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3873525</comments>
            <pubDate>Thu, 12 Aug 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">3873525</guid>        </item>
        <item>
            <title>Roles for Soluble Guanylate Cyclase and a Thiol Oxidation-Elicited Subunit Dimerization of Protein Kinase G in Pulmonary Artery Relaxation to Hydrogen Peroxide.</title>
            <link>http://www.medworm.com/index.php?rid=3873524&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%3D20709865%26dopt%3DAbstract</link>
            <description>Authors: Neo BH, Kandhi S, Wolin MS
    We have previously provided evidence that hydrogen peroxide (H(2)O(2)) stimulates soluble guanylate cyclase under conditions where it relaxes isolated endothelium-removed bovine pulmonary arteries (BPA). Since it was recently reported that H(2)O(2) induces coronary vasorelaxation associated with a NO/cGMP-independent thiol oxidation/subunit dimerization-elicited activation of protein kinase G (PKG), we investigated if this mechanism participates in the relaxation of BPA to H(2)O(2). BPA precontracted with serotonin (incubated under hypoxia to lower endogenous H(2)O(2)) were exposed to increasing concentrations of H(2)O(2). It was observed that 0.1-1 mM H(2)O(2) caused increased PKG dimerization and relaxation. These responses were associated with inc...</description>
            <author>Am J Physiol Heart C...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3873524</comments>
            <pubDate>Thu, 12 Aug 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">3873524</guid>        </item>
        <item>
            <title>Suppression of Circulating Free Fatty Acids with Acipimox in Chronic Heart Failure Patients Changes Whole Body Metabolism but Does not Affect Cardiac Function.</title>
            <link>http://www.medworm.com/index.php?rid=3873523&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%3D20709866%26dopt%3DAbstract</link>
            <description>Conclusion: Acipimox caused minor changes in whole body metabolism and decreased FFA supply, but a long-term reduction in circulating FFA with acipimox did not change systolic or diastolic cardiac function or exercise capacity in patients with HF.
    PMID: 20709866 [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=3873523</comments>
            <pubDate>Thu, 12 Aug 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">3873523</guid>        </item>
        <item>
            <title>Ionic Mechanisms of Electrophysiological Heterogeneity and Conduction Block in the Infarct Border Zone.</title>
            <link>http://www.medworm.com/index.php?rid=3873522&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%3D20709867%26dopt%3DAbstract</link>
            <description>Authors: Decker KF, Rudy Y
    Increased incidence of arrhythmia in the healing phase post-infarction has been linked to remodeling in the epicardial border zone (EBZ). Ionic models of normal zone (NZ) and EBZ myocytes were incorporated into one-dimensional models of propagation to gain mechanistic insight into how ion channel remodeling affects AP duration (APD) and refractoriness, vulnerability to conduction block and conduction safety post-infarction. We find that EBZ tissue exhibits abnormal APD restitution. Remodeled I(Na) and I(CaL) promote increased ERP and prolonged APD at short diastolic interval (DI). While post-repolarization refractoriness (PRR) due to remodeled EBZ I(Na) is the primary determinant of the vulnerable window (VW) for conduction block at the NZ to EBZ transition i...</description>
            <author>Am J Physiol Heart C...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3873522</comments>
            <pubDate>Thu, 12 Aug 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">3873522</guid>        </item>
        <item>
            <title>Tumor necrosis factor inhibitors as novel therapeutic tools for vascular remodeling diseases.</title>
            <link>http://www.medworm.com/index.php?rid=3873521&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%3D20709868%26dopt%3DAbstract</link>
            <description>CONCLUSION: We demonstrate for the first time that inhibition of the TNF/Akt/HIF-1 axis prevents vascular remodeling. TNF inhibitors may therefore represent new and interesting therapeutic tools against VRD.
    PMID: 20709868 [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=3873521</comments>
            <pubDate>Thu, 12 Aug 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">3873521</guid>        </item>
        <item>
            <title>Cardiac oxytocin receptor blockade stimulates adverse cardiac remodeling in ovariectomized spontaneously hypertensive rats.</title>
            <link>http://www.medworm.com/index.php?rid=3806509&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%3D20671291%26dopt%3DAbstract</link>
            <description>In conclusion, these results demonstrate that cardiac OTRs are involved in the regulation of cardiac function of OVX SHRs. The decreases of OTRs may contribute to cardiac pathology following menopause.
    PMID: 20671291 [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=3806509</comments>
            <pubDate>Sat, 31 Jul 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">3806509</guid>        </item>
        <item>
            <title>The Roles of Cytosolic Ca2+ Concentration and Myofilament Ca2+ Sensitization in Age-Dependent Cerebrovascular Myogenic Tone.</title>
            <link>http://www.medworm.com/index.php?rid=3767900&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%3D20639216%26dopt%3DAbstract</link>
            <description>Authors: Charles SM, Zhang L, Cipolla MJ, Buchholz JN, Pearce WJ
    In light of evidence that immature arteries contain a higher proportion of non-contractile smooth muscle cells than found in fully differentiated mature arteries, the present study explores the hypothesis that age-related differences in smooth muscle phenotype contribute to age-related differences in contractility. Because Ca(2+) handling differs markedly between contractile and non-contractile smooth muscle, the present studies specifically test the hypothesis that the relative contributions of calcium influx and myofilament sensitization to myogenic tone are upregulated, whereas Ca(2+) release is downregulated, in immature (P14) compared to mature (6-month-old) rat middle cerebral arteries (MCA). Myofilament Ca(2+) sens...</description>
            <author>Am J Physiol Heart C...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3767900</comments>
            <pubDate>Thu, 15 Jul 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">3767900</guid>        </item>
        <item>
            <title>Stretch-induced hypertrophy of isolated adult rabbit cardiomyocytes.</title>
            <link>http://www.medworm.com/index.php?rid=3767899&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%3D20639217%26dopt%3DAbstract</link>
            <description>This study clearly indicates that cyclic stretch is a strong, direct trigger to induce hypertrophy in fully differentiated rabbit cardiomyocytes. The present findings do not support the notion that stretch-mediated hypertrophy of adult rabbit cardiomyocytes involves autocrine/paracrine actions of AngII, TGFbeta1 or IGF-I.
    PMID: 20639217 [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=3767899</comments>
            <pubDate>Thu, 15 Jul 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">3767899</guid>        </item>
        <item>
            <title>Interleukin-10 inhibits the in vivo and in vitro adverse effects of TNF-{alpha} on the endothelium of murine aorta.</title>
            <link>http://www.medworm.com/index.php?rid=3767898&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%3D20639218%26dopt%3DAbstract</link>
            <description>Conclusion: The anti-inflammatory cytokine IL-10 prevents impairment in endothelium- dependent vasorelaxation caused by TNF-alpha by preserving eNOS expression.
    PMID: 20639218 [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=3767898</comments>
            <pubDate>Thu, 15 Jul 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">3767898</guid>        </item>
        <item>
            <title>Observations of time-based measures of flow-mediated dilation of forearm conduit arteries: Implications for the accurate assessment of endothelial function.</title>
            <link>http://www.medworm.com/index.php?rid=3767897&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%3D20639219%26dopt%3DAbstract</link>
            <description>In conclusion, although time to-FMD(max) does not appear to be a useful adjunctive measure of endothelial health, the use of continuous diameter measurements provides important data in the study of endothelial function in healthy subjects and patients with cardiovascular disease.
    PMID: 20639219 [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=3767897</comments>
            <pubDate>Thu, 15 Jul 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">3767897</guid>        </item>
        <item>
            <title>Pulmonary and Systemic Vasodilator Responses to the Soluble Guanylyl Cyclase Stimulator, Bay 41-8543, are Modulated by Nitric Oxide.</title>
            <link>http://www.medworm.com/index.php?rid=3767896&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%3D20639220%26dopt%3DAbstract</link>
            <description>Authors: Badejo AM, Nossaman VE, Pankey EA, Bhartiya M, Kannadka CB, Murthy SN, Nossaman BD, Kadowitz PJ
    Bay 41-8543 is a nitric oxide (NO)-independent stimulator of soluble guanylyl cyclase (sGC). Responses to iv injections of BAY 41-8543 were investigated under baseline and elevated tone conditions, and when NO synthase (NOS) was inhibited with L-NAME. Under baseline conditions, iv injections of BAY 41-8543 caused small decreases in pulmonary arterial pressure, larger decreases in systemic arterial pressure, and increases in cardiac output. When pulmonary arterial pressure was increased to approximately 30 mm Hg with an iv infusion of U46619, iv injections of BAY 41-8543 produced larger dose-dependent decreases in pulmonary arterial pressure, and the relative decreases in pulmonary a...</description>
            <author>Am J Physiol Heart C...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3767896</comments>
            <pubDate>Thu, 15 Jul 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">3767896</guid>        </item>
        <item>
            <title>Cardiac overexpression of the human 5-HT4 receptor in mice.</title>
            <link>http://www.medworm.com/index.php?rid=3767895&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%3D20639221%26dopt%3DAbstract</link>
            <description>Authors: Gergs U, Baumann M, BÃ¶ckler A, Buchwalow IB, Ebelt H, Fabritz L, Hauptmann S, Keller N, Kirchhof P, Klockner U, PÃ¶nicke K, Rueckschloss U, Schmitz W, Werner F, Neumann J
    Serotonin (5-HT) exerts pleiotropic effects in the human cardiovascular system. Some of the effects are thought to be mediated via 5-HT(4)-receptors, which are expressed in the human atrium and in ventricular tissue. However, a true animal model to study these receptors in more detail is hitherto lacking. Therefore, we generated for the first time a transgenic mouse (TG) with cardiac myocyte specific expression of the human 5-HT(4)-receptor. RT-PCR and immunohistochemistry revealed expression of the receptor on mRNA and protein level. Stimulation of isolated cardiac preparations by isoproterenol increase...</description>
            <author>Am J Physiol Heart C...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3767895</comments>
            <pubDate>Thu, 15 Jul 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">3767895</guid>        </item>
        <item>
            <title>Upregulation of nox1 in vascular smooth muscle leads to impaired endothelium-dependent relaxation via enos uncoupling.</title>
            <link>http://www.medworm.com/index.php?rid=3767892&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%3D20639222%26dopt%3DAbstract</link>
            <description>UPREGULATION OF NOX1 IN VASCULAR SMOOTH MUSCLE LEADS TO IMPAIRED ENDOTHELIUM-DEPENDENT RELAXATION VIA ENOS UNCOUPLING.
    Am J Physiol Heart Circ Physiol. 2010 Jul 16;
    Authors: Dikalova AE, Gongora MC, Harrison DG, Lambeth JD, Dikalov S, Griendling KK
    Recent work has made it clear that oxidant systems interact. To investigate potential cross-talk between Nox1 upregulation in vascular smooth muscle and endothelial function, transgenic mice overexpressing Nox1 in smooth muscle cells (Tg(SMCnox1)) were subjected to angiotensin II (Ang II)-induced hypertension. As expected, NADPH-dependent superoxide generation was increased in aortas from Nox1 overexpressing mice. Infusion of Ang II (0.7 mg/kg per day) for 2 weeks potentiated NADPH-dependent superoxide generation and hydrogen peroxid...</description>
            <author>Am J Physiol Heart C...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3767892</comments>
            <pubDate>Thu, 15 Jul 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">3767892</guid>        </item>
        <item>
            <title>Am J Physiol Heart Circ Physiol; +40 new citations</title>
            <link>http://www.medworm.com/index.php?rid=3737532&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%252F07%252F01%252000.36%2522%255BMHDA%255D%253A%25222010%252F07%252F09%252010.03%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%252F07%252F01%252000.36%2522%255BEDAT%255D%29%29</link>
            <description>40 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 2010/07/09PubMed, 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=3737532</comments>
            <pubDate>Fri, 09 Jul 2010 14:03:02 +0100</pubDate>
            <guid isPermaLink="false">3737532</guid>        </item>
        <item>
            <title>Am J Physiol Heart Circ Physiol; +64 new citations</title>
            <link>http://www.medworm.com/index.php?rid=3696026&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%252F06%252F22%252014.21%2522%255BMHDA%255D%253A%25222010%252F06%252F25%252009.30%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%252F06%252F22%252014.21%2522%255BEDAT%255D%29%29</link>
            <description>64 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 2010/06/25PubMed, 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=3696026</comments>
            <pubDate>Fri, 25 Jun 2010 13:30:03 +0100</pubDate>
            <guid isPermaLink="false">3696026</guid>        </item>
        <item>
            <title>Am J Physiol Heart Circ Physiol; +16 new citations</title>
            <link>http://www.medworm.com/index.php?rid=3677448&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%252F06%252F10%252011.48%2522%255BMHDA%255D%253A%25222010%252F06%252F19%252019.12%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%252F06%252F10%252011.48%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 2010/06/19PubMed, 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=3677448</comments>
            <pubDate>Sat, 19 Jun 2010 23:12:12 +0100</pubDate>
            <guid isPermaLink="false">3677448</guid>        </item>
        <item>
            <title>Endotoxin impairs cardiac hemodynamics by affecting loading conditions but not by reducing cardiac inotropism.</title>
            <link>http://www.medworm.com/index.php?rid=3648356&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%3D20525873%26dopt%3DAbstract</link>
            <description>Authors: Li J, Rosenblatt-Velin N, Loukili N, Pacher P, Feihl F, Waeber B, Liaudet L
    Acute myocardial dysfunction is a typical manifestation of septic shock. Experimentally, the administration of endotoxin (lipopolysacharride, LPS) to laboratory animals is frequently used to study such dysfunction. However, a majority of studies used load-dependent indices of cardiac function (including ejection fraction, EF, and maximal systolic pressure increment, dp/dt max), which do not directly explore cardiac inotropism. Therefore, we evaluated the direct effects of LPS on myocardial contractility, using left ventricular (LV) pressure-volume catheters in mice. Male BALB/c mice received an intraperitoneal injection of E. Coli LPS (1, 5, 10, or 20 mg/kg). After 2, 6 or 20 h, cardiac function was an...</description>
            <author>Am J Physiol Heart C...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3648356</comments>
            <pubDate>Thu, 03 Jun 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">3648356</guid>        </item>
        <item>
            <title>Transmural Heterogeneity of Repolarization and Ca2+ Handling in a Model of Mouse Ventricular Tissue.</title>
            <link>http://www.medworm.com/index.php?rid=3648355&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%3D20525874%26dopt%3DAbstract</link>
            <description>Authors: Bondarenko VE, Rasmusson RL
    Mouse hearts have a diversity of action potentials (APs) generated by the cardiac myocytes from different regions. Recent evidence shows that cells from the epicardial and endocardial regions of the mouse ventricle have diversity in calcium handling properties as well as potassium current expression. In order to examine mechanisms of AP generation, propagation, and stability in transmurally heterogeneous tissue we developed a comprehensive model of the mouse cardiac cells from the epicardial and endocardial regions of the heart. Our computer model simulates the following differences between epicardial and endocardial myocytes: 1) action potential duration is longer in endocardial and shorter in epicardial myocytes; 2) diastolic and systolic [Ca(2+)]...</description>
            <author>Am J Physiol Heart C...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3648355</comments>
            <pubDate>Thu, 03 Jun 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">3648355</guid>        </item>
        <item>
            <title>eNOS is Required for Acute in vivo Ischemic Preconditioning of the Heart: Effects of Ischemic Duration and Gender.</title>
            <link>http://www.medworm.com/index.php?rid=3648354&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%3D20525875%26dopt%3DAbstract</link>
            <description>In conclusion, IPC protects WT mice against in vivo myocardial IR injury regardless of gender and ischemic duration, but, deletion of eNOS abolishes the cardioprotective effect of classical IPC.
    PMID: 20525875 [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=3648354</comments>
            <pubDate>Thu, 03 Jun 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">3648354</guid>        </item>
        <item>
            <title>Obestatin affords cardioprotection to the ischemic/reperfused isolated rat heart and inhibits apoptosis in cultures of similarly stressed cardiomyocytes.</title>
            <link>http://www.medworm.com/index.php?rid=3648353&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%3D20525876%26dopt%3DAbstract</link>
            <description>Authors: Alloatti G, Arnoletti E, Bassino E, Penna C, Perrelli MG, GhÃ© C, Muccioli G
    Obestatin, a newly discovered peptide encoded by the ghrelin gene, induces expression of genes regulating pancreatic beta-cell differentiation, insulin biosynthesis and glucose metabolism. It also activates anti-apoptotic signalling pathways such as PI3K and ERK1/2 in pancreatic beta-cells and human islets. Since these kinases have been shown to protect against myocardial injury, we sought to investigate whether obestatin would exert cardioprotective effects. Both isolated perfused rat heart and cultured cardiomyocyte models of ischemia/reperfusion (I/R) were used, measuring infarct size and cell apoptosis as end points of injury. The presence of specific obestatin receptors on cardiac cells, as wel...</description>
            <author>Am J Physiol Heart C...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3648353</comments>
            <pubDate>Thu, 03 Jun 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">3648353</guid>        </item>
        <item>
            <title>Functional anatomy of the murine sinus node: high-resolution optical mapping of ankyrin-b heterozygous mice.</title>
            <link>http://www.medworm.com/index.php?rid=3648352&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%3D20525877%26dopt%3DAbstract</link>
            <description>FUNCTIONAL ANATOMY OF THE MURINE SINUS NODE: HIGH-RESOLUTION OPTICAL MAPPING OF ANKYRIN-B HETEROZYGOUS MICE.
    Am J Physiol Heart Circ Physiol. 2010 Jun 4;
    Authors: Glukhov AV, Fedorov VV, Anderson ME, Mohler PJ, Efimov IR
    The mouse is widely used as the genetic platform for investigating the molecular mechanisms of sinoatrial node (SAN) pacemaking. Recently, it was shown that isolated SAN cells from the ankyrin-B deficient mice displayed severe pacemaking dysfunction similar to individuals harboring the ANK2 allele variants. However, these results have been limited to isolated SAN cells only and thus did not evaluate the functional anatomy of the widely distributed atrial pacemaker complex. We studied pacemaker function in an intact mouse atrial preparation, which included the S...</description>
            <author>Am J Physiol Heart C...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3648352</comments>
            <pubDate>Thu, 03 Jun 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">3648352</guid>        </item>
        <item>
            <title>Myocardial contractile response to physiological stress improves with high saturated fat feeding in heart failure.</title>
            <link>http://www.medworm.com/index.php?rid=3618490&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%3D20511406%26dopt%3DAbstract</link>
            <description>Authors: Berthiaume JM, Bray MS, McElfresh TA, Chen X, Azam SM, Young ME, Hoit BD, Chandler MP
    Impaired myocardial contractile function is a hallmark of heart failure (HF) which may present under resting conditions and/or during physiological stress. Previous studies reported that high fat feeding in mild-moderate heart failure/LV dysfunction is associated with improved contractile function at baseline. The goal of this study was to determine whether myocardial function is compromised in response to physiological stress and to evaluate the global gene expression profile of rats fed high dietary fat following infarction. Male Wistar rats underwent ligation or sham surgery and fed normal (10% kcal fat) (SHAM+NC, HF+NC) or high fat (60% kcal saturated fat) (SHAM+SAT, HF+SAT) for 8 weeks. ...</description>
            <author>Am J Physiol Heart C...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3618490</comments>
            <pubDate>Thu, 27 May 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">3618490</guid>        </item>
        <item>
            <title>Ethnic differences in resistance artery contractility of normotensive pregnant women.</title>
            <link>http://www.medworm.com/index.php?rid=3618489&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%3D20511407%26dopt%3DAbstract</link>
            <description>Authors: Brewster LM, Taherzadeh Z, Volger S, Clark JF, Rolf T, Wolf H, van Bavel E, van Montfrans GA
    Black women are at greater risk to develop hypertension during pregnancy, with a 4.5 times higher rate of fatal preeclampsia as compared to white women. Therefore, it is important to identify factors that may affect this risk. Our group previously proposed that high activity of the central regulatory enzyme of energy metabolism, creatine kinase (CK), may increase ATP buffer capacity and lead to enhanced vascular contractility and reduced NO bioavailability. Therefore, we assessed microvascular contractility characteristics in isolated resistance arteries from self-defined black and white normotensive pregnant women, using a Mulvany-Halpern myograph. Additionally, morphology was assesse...</description>
            <author>Am J Physiol Heart C...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3618489</comments>
            <pubDate>Thu, 27 May 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">3618489</guid>        </item>
        <item>
            <title>Editorial Focus : The Danger of Sedenterism- Endothelium at Risk.</title>
            <link>http://www.medworm.com/index.php?rid=3618488&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%3D20511408%26dopt%3DAbstract</link>
            <description>Authors: Widlansky ME
    n/a.
    PMID: 20511408 [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=3618488</comments>
            <pubDate>Thu, 27 May 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">3618488</guid>        </item>
        <item>
            <title>Central neuronal activation and pressor responses induced by circulating angiotensin II. Role of brain aldosterone-&quot;ouabain&quot; pathway.</title>
            <link>http://www.medworm.com/index.php?rid=3618487&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%3D20511409%26dopt%3DAbstract</link>
            <description>Central neuronal activation and pressor responses induced by circulating angiotensin II. Role of brain aldosterone-&quot;ouabain&quot; pathway.
    Am J Physiol Heart Circ Physiol. 2010 May 28;
    Authors: Huang BS, Ahmadi S, Ahmad M, White RA, Leenen FH
    An increase in plasma Ang II causes neuronal activation in hypothalamic nuclei and a slow pressor response presumably by increasing sympathetic drive. We evaluated whether activation of a neuromodulatory pathway, involving aldosterone-&quot;ouabain&quot;, is involved in these responses. In Wistar rats, subcutaneous infusion of Ang II at 150 and 500 ng/kg/min gradually increased blood pressure up to 60 mmHg at the highest dose. Ang II at 500 ng/kg/min increased plasma Ang II by 4 fold, plasma aldosterone 20 fold and hypothalamic aldosterone 3 fold. Intrac...</description>
            <author>Am J Physiol Heart C...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3618487</comments>
            <pubDate>Thu, 27 May 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">3618487</guid>        </item>
        <item>
            <title>Sustained Suppression of Sympathetic Activity and Arterial Pressure During Chronic Activation of the Carotid Baroreflex.</title>
            <link>http://www.medworm.com/index.php?rid=3618486&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%3D20511410%26dopt%3DAbstract</link>
            <description>Authors: Lohmeier TE, Iliescu R, Dwyer TM, Irwin E, Cates AW, Rossing MA
    Following sinoaortic denervation, which eliminates arterial baroreceptor input into the brain, there are slowly developing adaptations that abolish initial sympathetic activation and hypertension. In comparison, electrical stimulation of the carotid sinus for one week produces sustained reductions in sympathetic activity and arterial pressure. However, whether compensations occur subsequently to diminish these responses is unclear. Therefore, we determined whether there are important central and/or peripheral adaptations that diminish the sympathoinhibitory and blood pressure lowering effects of more sustained carotid sinus stimulation. To this end, we measured whole body plasma norepinephrine spillover and alpha-...</description>
            <author>Am J Physiol Heart C...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3618486</comments>
            <pubDate>Thu, 27 May 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">3618486</guid>        </item>
        <item>
            <title>A cardioprotective agent of a novel calpain inhibitor, SNJ-1945 exerts {beta}1-actions on left ventricular mechanical work and energetics.</title>
            <link>http://www.medworm.com/index.php?rid=3618485&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%3D20511411%26dopt%3DAbstract</link>
            <description>Authors: Yoshikawa Y, Zhang GX, Obata K, Matsuyoshi H, Asada K, Taniguchi S, Takaki M
    We have previously shown that a newly developed calpain inhibitor, SNJ-1945 (SNJ) with good aqueous solubility prevents the heart from KCl arrest-reperfusion injury associated with the impairment of total Ca(2+) handling by inhibiting the proteolysis of alpha-fodrin as a cardioplegia. The aim of the present study was to investigate certain actions of this calpain inhibitor, SNJ on left ventricular (LV) mechanical work and energetics in the cross-circulated excised rat hearts underwent blood perfusion with 40 muM SNJ. Mean end-systolic pressure at midrange LV volume (ESP(mLVV)) and systolic pressure-volume area (PVA) at mLVV (PVA(mLVV): a total mechanical energy per beat) were significantly increased b...</description>
            <author>Am J Physiol Heart C...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3618485</comments>
            <pubDate>Thu, 27 May 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">3618485</guid>        </item>
        <item>
            <title>Divergent effects of low O2 tension and iloprost on ATP release from erythrocytes of humans with type 2 diabetes: Implications for O2 supply to skeletal muscle.</title>
            <link>http://www.medworm.com/index.php?rid=3618484&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%3D20511412%26dopt%3DAbstract</link>
            <description>Authors: Sprague RS, Goldman DG, Bowles EA, Achilleus D, Stephenson AH, Ellis CG, Ellsworth ML
    Erythrocytes release both O(2) and a vasodilator, ATP, when exposed to reduced O(2) tension. We investigated the hypothesis that ATP release is impaired in erythrocytes of humans with type 2 diabetes (DM2) and that this defect compromises the ability of these cells to stimulate dilation of resistance vessels. We also determined if a general vasodilator, the prostacyclin analog, iloprost (ILO), stimulates ATP release from healthy human (HH) and DM2 erythrocytes. Finally, we used a computational model to compare the effect on tissue O(2) levels of increases in blood flow directed to areas of increased O(2) demand (erythrocyte ATP release) with non-directed increases in flow (ILO). HH erythrocyt...</description>
            <author>Am J Physiol Heart C...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3618484</comments>
            <pubDate>Thu, 27 May 2010 23:00:00 +0100</pubDate>
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        <item>
            <title>Increased inducible nitric oxide synthase and arginase II expression in heart failure: No net nitrite/nitrate production and protein S-nitrosylation.</title>
            <link>http://www.medworm.com/index.php?rid=3618483&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%3D20511413%26dopt%3DAbstract</link>
            <description>Conclusion: Concomitant increases in iNOS and arginase expression result in unchanged NO species and protein S-nitrosylation; with substrate limitation, uncoupled iNOS produces superoxide anions and contributes to contractile dysfunction.
    PMID: 20511413 [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=3618483</comments>
            <pubDate>Thu, 27 May 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">3618483</guid>        </item>
        <item>
            <title>Long-term exercise training does not alter brachial and femoral artery vasomotor function and endothelial phenotype in healthy pigs.</title>
            <link>http://www.medworm.com/index.php?rid=3618482&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%3D20511414%26dopt%3DAbstract</link>
            <description>Authors: Padilla J, Newcomer SC, Simmons GH, Kreutzer KV, Laughlin MH
    While the beneficial effects of exercise training on conduit artery endothelial function are well established in animals and humans with compromised basal function, whether or not exercise exerts favorable effects on a healthy endothelium is inconclusive. We sought to determine whether long-term exercise training enhances endothelial function in peripheral conduit arteries of healthy pigs. Using a retrospective analysis of data collected in our laboratory (n=127), we compared in-vitro brachial and femoral artery endothelium-dependent and independent relaxation between a group of pigs that exercise-trained for 16-20 weeks and a group that remained sedentary. No differences in vasomotor function were found between the ...</description>
            <author>Am J Physiol Heart C...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3618482</comments>
            <pubDate>Thu, 27 May 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">3618482</guid>        </item>
        <item>
            <title>Human thoracic duct in vitro: diameter-tension properties, spontaneous and evoked contractile activity.</title>
            <link>http://www.medworm.com/index.php?rid=3618481&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%3D20511415%26dopt%3DAbstract</link>
            <description>Authors: Telinius N, Drewsen N, Pilegaard H, Deleval M, Aalkjaer C, Hjortdal VE, Boedtkjer DM
    The current study characterizes the mechanical properties of the human thoracic duct and demonstrates a role for adrenoceptors, thromboxane and endothelin receptors in human lymph vessel function. With ethical permission and informed consent, portions of the thoracic duct (2-5cm) were resected and retrieved at T7-T9 during esophageal and cardia cancer surgery. Ring segments (2mm long) were mounted in a myograph for isometric tension (Newton/meter) measurement. The diameter-tension relationship was established using ducts from 10 individuals. Peak active tension of 6.24+/-0.75N/m was observed with a corresponding passive tension of 3.11+/-0.67N/m and average internal diameter of 2.21mm. The equ...</description>
            <author>Am J Physiol Heart C...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3618481</comments>
            <pubDate>Thu, 27 May 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">3618481</guid>        </item>
        <item>
            <title>TGF-beta impairs vasomotor function by activation of NADPH oxidase driven superoxide production leading to hypertension in apoE-/- mice.</title>
            <link>http://www.medworm.com/index.php?rid=3618480&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%3D20511416%26dopt%3DAbstract</link>
            <description>Conclusion: Our results demonstrate that elevated circulating TGF-ss1 cause endothelial dysfunction through NADPH oxidase activation-induced oxidative stress accelerating atherosclerosis and hypertension in apoE(-/-) mice. These findings may provide a mechanism explaining accelerated atherosclerosis in patients with elevated plasma TGF-beta(1).
    PMID: 20511416 [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=3618480</comments>
            <pubDate>Thu, 27 May 2010 23:00:00 +0100</pubDate>
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        <item>
            <title>Am J Physiol Heart Circ Physiol; +37 new citations</title>
            <link>http://www.medworm.com/index.php?rid=3586297&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%252F05%252F18%252012.09%2522%255BMHDA%255D%253A%25222010%252F05%252F21%252018.06%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%252F05%252F18%252012.09%2522%255BEDAT%255D%29%29</link>
            <description>37 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 2010/05/21PubMed, 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=3586297</comments>
            <pubDate>Fri, 21 May 2010 22:06:02 +0100</pubDate>
            <guid isPermaLink="false">3586297</guid>        </item>
        <item>
            <title>Enforced Physical Inactivity Increases Endothelial Microparticle Levels in Healthy Volunteers.</title>
            <link>http://www.medworm.com/index.php?rid=3574042&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%3D20472757%26dopt%3DAbstract</link>
            <description>In conclusion, the endothelium should be the focus of special care in situations of acute limitation of physical activity.
    PMID: 20472757 [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=3574042</comments>
            <pubDate>Thu, 13 May 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">3574042</guid>        </item>
        <item>
            <title>X-linked inhibitor of apoptosis protein controls integrin {alpha}5-mediated cell adhesion and migration.</title>
            <link>http://www.medworm.com/index.php?rid=3574041&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%3D20472758%26dopt%3DAbstract</link>
            <description>In this study, we demonstrated that XIAP is recruited into the integrin alpha5 complex via caveolin-1 binding, and mediates cell adhesion. We also determined that XIAP is critical to shear stress-stimulated extracellular signal-regulated kinase (ERK) activation in an integrin alpha5-dependent manner, but is not important to VEGF-induced ERK activation. This differential activation of ERK is partly attributable to unique localizations of the receptors. Furthermore, we confirmed that XIAP is an essential molecule in the efficient recruitment of focal adhesion kinase (FAK) into the integrin alpha5-associated complex. This integrin alpha5-caveolin-1-XIAP-FAK multicomplex regulates endothelial cell migration via a mechanism that involves shear-dependent ERK activation. Together, our results ind...</description>
            <author>Am J Physiol Heart C...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3574041</comments>
            <pubDate>Thu, 13 May 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">3574041</guid>        </item>
        <item>
            <title>Short-term Disruption in Regional Left Ventricular Electrical Conduction Patterns Increases Interstitial Matrix Metalloproteinase Activity.</title>
            <link>http://www.medworm.com/index.php?rid=3574040&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%3D20472759%26dopt%3DAbstract</link>
            <description>This study demonstrates that despite restoration of mechanical function, disturbances in electrical conduction - in and of itself - can cause acute increases in regional in vivo MMP activation, and therefore, contribute to myocardial remodeling.
    PMID: 20472759 [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=3574040</comments>
            <pubDate>Thu, 13 May 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">3574040</guid>        </item>
        <item>
            <title>Importance of lymph vessels in transcapillary fluid balance in gingiva studied in a transgenic mouse model.</title>
            <link>http://www.medworm.com/index.php?rid=3574039&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%3D20472760%26dopt%3DAbstract</link>
            <description>Authors: Mkonyi LE, Bletsa A, Fristad I, Wiig H, Berggreen E
    Gingiva is frequently challenged by oral bacterial products leading to inflammatory responses such as increased fluid filtration and edema formation. The role of initial lymphatics for transcapillary fluid balance in gingiva is unknown and was therefore investigated in genetically engineered K14-VEGFR-3-Ig (K14) lymphedema mice. The mutant mice demonstrated a total lack of lymphatics in gingiva, whereas lymphatics were found in the submucosal parts of alveolar mucosa although almost completely absent in mucosa. In wild-type (WT) mice, lymphatic vessels were detected in mucosal and submucosal part of alveolar mucosa. Interstitial fluid pressure (P(if)) measured with micropipettes was increased in gingiva of K14 mice in the nor...</description>
            <author>Am J Physiol Heart C...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3574039</comments>
            <pubDate>Thu, 13 May 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">3574039</guid>        </item>
        <item>
            <title>Transgenic Overexpression of Pregnancy-Associated Plasma Protein-A in Murine Arterial Smooth Muscle Accelerates Atherosclerotic lesion Development.</title>
            <link>http://www.medworm.com/index.php?rid=3574038&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%3D20472761%26dopt%3DAbstract</link>
            <description>Authors: Conover CA, Mason MA, Bale LK, Harrington SC, Nyegaard M, Oxvig C, Overgaard MT
    Pregnancy-associated plasma protein-A (PAPP-A) increases local insulin-like growth factor (IGF)-I bioavailability through cleavage of inhibitory IGF binding protein (IGFBP)-4 in a variety of systems, including the cardiovascular system. To test the hypothesis that expression of PAPP-A promotes the development of atherosclerotic lesions, we generated transgenic mice that express human PAPP-A in arterial smooth muscle. Four founder lines were characterized for transgenic human PAPP-A mRNA and protein expression, IGFBP-4 protease activity, and tissue specificity. In Study I, apolipoprotein E knock-out (ApoE KO) mice, a well characterized mouse model of atherosclerosis, and ApoE KO mice expressing the ...</description>
            <author>Am J Physiol Heart C...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3574038</comments>
            <pubDate>Thu, 13 May 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">3574038</guid>        </item>
        <item>
            <title>Editorial Focus - Endothelial Nrf2 activation: a new target for resveratrol?</title>
            <link>http://www.medworm.com/index.php?rid=3574037&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%3D20472762%26dopt%3DAbstract</link>
            <description>Authors: Hasko G, Pacher P
    N/A.
    PMID: 20472762 [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=3574037</comments>
            <pubDate>Thu, 13 May 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">3574037</guid>        </item>
        <item>
            <title>The mechanism by which Rho A regulates vascular reactivity after hemorrhagic shock in rats.</title>
            <link>http://www.medworm.com/index.php?rid=3574036&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%3D20472763%26dopt%3DAbstract</link>
            <description>Conclusion RhoA has an important role in the regulation of vascular reactivity after hemorrhagic shock. The Rho kinase-myosin light chain phosphatase and Rac1-PAK-myosin light chain kinase signal pathways participate in the regulatory process of RhoA. Rho kinase-myosin light chain phosphatase may be the main signaling pathway by which RhoA regulates vascular reactivity.
    PMID: 20472763 [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=3574036</comments>
            <pubDate>Thu, 13 May 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">3574036</guid>        </item>
        <item>
            <title>Role of lysyl oxidase in myocardial fibrosis. From basic science to clinical aspects.</title>
            <link>http://www.medworm.com/index.php?rid=3574035&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%3D20472764%26dopt%3DAbstract</link>
            <description>Authors: LÃ³pez B, GonzÃ¡lez A, Hermida N, Valencia F, de Teresa E, Diez J
    Due to its dynamic nature, the composition and structure of the myocardial collagen network can be reversibly modified to adapt to transient cardiac injuries. In response to persistent injury however, irreversible, maladaptive changes of the network occur leading to fibrosis mostly characterized by the excessive interstitial and perivascular deposition of collagen types I and III fibers. It is now becoming apparent that myocardial fibrosis directly contributes to adverse myocardial remodeling and the resulting alterations of left ventricular (LV) anatomy and function present in the major types of cardiac diseases. The enzyme lysyl oxidase (LOX) is a cupper-dependent extracellular enzyme that catalyzes lysine...</description>
            <author>Am J Physiol Heart C...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3574035</comments>
            <pubDate>Thu, 13 May 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">3574035</guid>        </item>
        <item>
            <title>Apparent PKA Activity Responds to Intermittent Hypoxia in Bone Cells: A Redox Pathway?</title>
            <link>http://www.medworm.com/index.php?rid=3549865&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%3D20453101%26dopt%3DAbstract</link>
            <description>Authors: Zhang YL, Tavakoli H, Chachisvilis M
    We have studied hypoxia induced dynamic changes in the balance between PKA (protein kinase A) and its counteracting phosphatases in micro fluidic environment in single cells using picosecond fluorescence spectroscopy and intramolecular fluorescence resonance energy transfer (FRET) based sensor of PKA activity. (i) We have found that the apparent PKA activity in bone cells (MC3T3-E1) and in endothelial cells (BAEC) is rapidly and sensitively modulated by level of oxygen in the media. When oxygen concentration in the glucose containing media is lowered due to oxygen consumption by the cells in the micro fluidic chamber, the apparent PKA activity increases; reoxygenation of cells under hypoxia leads to rapid (~2 min) decrease of apparent PKA a...</description>
            <author>Am J Physiol Heart C...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3549865</comments>
            <pubDate>Thu, 06 May 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">3549865</guid>        </item>
        <item>
            <title>Sex differences in mechanisms of cardiac excitation-contraction coupling in rat ventricular myocytes.</title>
            <link>http://www.medworm.com/index.php?rid=3549864&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%3D20453102%26dopt%3DAbstract</link>
            <description>Authors: Farrell SR, Ross JL, Howlett SE
    Components of cardiac excitation-contraction (EC)-coupling were compared in ventricular myocytes isolated from 3-month-old male and female rats. Calcium concentrations (fura-2) and cell shortening (edge-detector) were measured simultaneously at 37 degrees C. Membrane potential and ionic currents were measured with microelectrodes. Action potentials were similar in male and female myocytes, but contractions were smaller and slower in females. In voltage-clamped cells, peak contractions were smaller in females than males (5.1 +/- 0.7 vs. 7.7 +/- 0.8 % diastolic length; p&amp;lt;0.05). Similarly, calcium transients were smaller in females than in males and the rate of rise of the calcium transient was slower in females. Despite smaller contractions and...</description>
            <author>Am J Physiol Heart C...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3549864</comments>
            <pubDate>Thu, 06 May 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">3549864</guid>        </item>
        <item>
            <title>Editorial Focus: Vascular receptors as new substrates for matrix metalloproteinases in hypertension and other inflammatory states.</title>
            <link>http://www.medworm.com/index.php?rid=3487492&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%3D20400684%26dopt%3DAbstract</link>
            <description>Authors: Kalogeris TJ, Korthuis RJ
    n/a.
    PMID: 20400684 [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=3487492</comments>
            <pubDate>Thu, 15 Apr 2010 23:00:00 +0100</pubDate>
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        <item>
            <title>Involvement of A1 adenosine receptors in altered vascular responses and inflammation in an allergic mouse model of asthma.</title>
            <link>http://www.medworm.com/index.php?rid=3487491&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%3D20400685%26dopt%3DAbstract</link>
            <description>In conclusion, allergic A(1)WT mice showed altered vascular reactivity, increased airway responsiveness and systemic inflammation. These data suggest that A(1) AR is pro-inflammatory systemically in this model of asthma.
    PMID: 20400685 [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=3487491</comments>
            <pubDate>Thu, 15 Apr 2010 23:00:00 +0100</pubDate>
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        <item>
            <title>Evidence for a Role of Opioids in Epoxyeicosatrienoic Acid (EET)-induced Cardioprotection in Rat Hearts.</title>
            <link>http://www.medworm.com/index.php?rid=3487490&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%3D20400686%26dopt%3DAbstract</link>
            <description>Authors: Gross GJ, Baker JE, Hsu A, Wu HE, Falck JR, Nithipatikom K
    We previously demonstrated that 11,12 and 14,15-epoxyeicosatrienoic acids (EETs) produce reductions in myocardial infarct size. Since a recent study demonstrated the release of opioids, in mediating the antinociceptive effect of 14,15-EET, we hypothesized that endogenous opioids may also be involved in mediating the cardioprotective effect of the EETs. To test this hypothesis, we used an in vivo rat model of infarction and a rat Langendorff model. In the infarct model, hearts were subjected to 30-min occlusion of left coronary artery and 2-hr reperfusion. Animals were treated with 11,12-EET or 14,15-EET (2.5 mg/kg) alone 15 min prior to occlusion or with opioid antagonists (naloxone, naltrindole, nor-BNI, and CTOP, a n...</description>
            <author>Am J Physiol Heart C...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3487490</comments>
            <pubDate>Thu, 15 Apr 2010 23:00:00 +0100</pubDate>
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        <item>
            <title>Transient stiffening of mitral valve leaflets in the beating heart.</title>
            <link>http://www.medworm.com/index.php?rid=3487489&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%3D20400687%26dopt%3DAbstract</link>
            <description>TRANSIENT STIFFENING OF MITRAL VALVE LEAFLETS IN THE BEATING HEART.
    Am J Physiol Heart Circ Physiol. 2010 Apr 16;
    Authors: Krishnamurthy G, Itoh A, Swanson JC, Miller DC, Ingels NB
    Anterior mitral leaflet stiffness during isovolumic contraction (IVC) is much greater than that during isovolumic relaxation (IVR). We have hypothesized that this stiffening is due to transient early-systolic force development in the slip of cardiac myocytes in the annular third of the anterior leaflet. Because the atrium is excited before IVC and leaflet myocytes contract for &amp;lt;/=250msec, this hypothesis predicts that IVC leaflet stiffness will drop to near-IVR values in the latter half of ventricular systole. We tested this prediction using radiopaque markers and inverse finite element analysis o...</description>
            <author>Am J Physiol Heart C...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3487489</comments>
            <pubDate>Thu, 15 Apr 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">3487489</guid>        </item>
        <item>
            <title>Vascular Hypertrophy-associated Hypertension of Profilin1 Transgenic Mouse Model Leads to Functional Remodeling of Peripheral Arteries.</title>
            <link>http://www.medworm.com/index.php?rid=3487488&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%3D20400688%26dopt%3DAbstract</link>
            <description>Authors: Hassona MD, Abouelnaga ZA, Elnakish MT, Awad MM, Alhaj M, Goldschmidt-Clermont PJ, Hassanain HH
    Increased mechanical stress/hypertension in the vessel wall triggers the hypertrophic signaling pathway, resulting in structural remodeling of vasculature. Vascular hypertrophy of resistance vessels leads to reduced compliance and elevation of blood pressure. We showed before that increased expression of profilin1 protein in the medial layer of the aorta induces stress fiber formation, triggering the hypertrophic signaling resulting in vascular hypertrophy and, ultimately, hypertension in older mice. Our hypothesis is that profilin1 induced vascular hypertrophy in resistance vessels, which led to elevation of blood pressure, and both of which contributed to the modulation of vascula...</description>
            <author>Am J Physiol Heart C...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3487488</comments>
            <pubDate>Thu, 15 Apr 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">3487488</guid>        </item>
        <item>
            <title>Local Adenosine Receptor Blockade Accentuates the Sympathetic Responses to Fatiguing Exercise.</title>
            <link>http://www.medworm.com/index.php?rid=3487487&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%3D20400689%26dopt%3DAbstract</link>
            <description>Authors: Cui J, Leuenberger UA, Blaha C, Yoder J, Gao Z, Sinoway LI
    The role adenosine plays in evoking the exercise pressor reflex in humans remains controversial. We hypothesized that localized forearm adenosine receptor blockade would attenuate muscle sympathetic nerve activity (MSNA) responses to fatiguing handgrip exercise in humans. Blood pressure (Finometer), heart rate, and MSNA from peroneal nerve were assessed in 11 healthy young volunteers during fatiguing isometric handgrip, post-exercise circulatory occlusion (PECO), and passive muscle stretch during PECO. The protocol was performed before and after adenosine receptor blockade by local infusion of 40 mg aminophylline in saline via forearm Bier block (regional intravenous anesthesia). In the second experiment, the same amou...</description>
            <author>Am J Physiol Heart C...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3487487</comments>
            <pubDate>Thu, 15 Apr 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">3487487</guid>        </item>
        <item>
            <title>Electro-Mechanical Wavebreak in a Model of the Human Left Ventricle.</title>
            <link>http://www.medworm.com/index.php?rid=3487486&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%3D20400690%26dopt%3DAbstract</link>
            <description>Authors: Keldermann RH, Nash MP, Gelderblom H, Wang VY, Panfilov AV
    We introduce an integrative 3D electro-mechanical model of the left ventricle (LV) of the human heart. Electrical activity is represented by the ionic TP06 model for human cardiac cells, mechanical activity is represented by the NHS active contractile tension model and the exponential Guccione passive elasticity model. These models are embedded into an anatomical model of the LV that contains a detailed description of cardiac geometry and fiber orientation field. We demonstrate that fiber shortening and wall thickening during normal excitation were qualitatively similar to experimental recordings. We used this model to study the effect of mechano-electrical feedback via the stretch-activated channels on the stability o...</description>
            <author>Am J Physiol Heart C...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3487486</comments>
            <pubDate>Thu, 15 Apr 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">3487486</guid>        </item>
        <item>
            <title>Am J Physiol Heart Circ Physiol; +35 new citations</title>
            <link>http://www.medworm.com/index.php?rid=3468605&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%252F04%252F07%252013.26%2522%255BMHDA%255D%253A%25222010%252F04%252F15%252001.34%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%252F04%252F07%252013.26%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 2010/04/15PubMed, 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=3468605</comments>
            <pubDate>Thu, 15 Apr 2010 05:34:02 +0100</pubDate>
            <guid isPermaLink="false">3468605</guid>        </item>
        <item>
            <title>Am J Physiol Heart Circ Physiol; +17 new citations</title>
            <link>http://www.medworm.com/index.php?rid=3444050&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%252F04%252F03%252019.28%2522%255BMHDA%255D%253A%25222010%252F04%252F07%252013.26%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%252F04%252F03%252019.28%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 2010/04/07PubMed, 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=3444050</comments>
            <pubDate>Wed, 07 Apr 2010 17:26:02 +0100</pubDate>
            <guid isPermaLink="false">3444050</guid>        </item>
        <item>
            <title>Am J Physiol Heart Circ Physiol; +43 new citations</title>
            <link>http://www.medworm.com/index.php?rid=3435516&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%252F03%252F31%252002.02%2522%255BMHDA%255D%253A%25222010%252F04%252F03%252019.28%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%252F03%252F31%252002.02%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 2010/04/03PubMed, 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=3435516</comments>
            <pubDate>Sat, 03 Apr 2010 23:28:07 +0100</pubDate>
            <guid isPermaLink="false">3435516</guid>        </item>
        <item>
            <title>Weight Loss in Obese C57BL/6 Mice Limits Adventitial Expansion of Established Angiotensin II-induced Abdominal Aortic Aneurysms.</title>
            <link>http://www.medworm.com/index.php?rid=3395449&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%3D20304811%26dopt%3DAbstract</link>
            <description>Authors: Police SB, Putnam K, Thatcher SE, Batifoulier-Yiannikouris F, Daugherty A, Cassis LA
    Previous studies demonstrated that obesity increases inflammation in periaortic adipose tissue and promotes angiotensin II (AngII)-induced AAAs. We sought to determine if weight loss of obese C57BL/6 mice would influence the progression of established AAAs. Male C57BL/6 mice were fed a high fat diet (HF) for 4 months, and then infused with either saline or AngII (1,000 ng/kg/min) for 3 months. Mice with dilated suprarenal aortas at 28 days of AngII infusion were designated to groups fed the HF (HF/HF) or a low fat diet (LF, 10% kcal as fat; HF/LF) to induce weight loss for the last 2 months of infusions. Suprarenal aortic lumen diameters of obese mice were increased by AngII infusion at day 28...</description>
            <author>Am J Physiol Heart C...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3395449</comments>
            <pubDate>Fri, 19 Mar 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3395449</guid>        </item>
        <item>
            <title>Physical activity maintains aortic endothelium dependent relaxation in the obese, type 2 diabetic OLETF rat.</title>
            <link>http://www.medworm.com/index.php?rid=3395448&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%3D20304812%26dopt%3DAbstract</link>
            <description>Authors: Bunker AK, Arce-Esquivel AA, Rector RS, Booth FW, Ibdah JA, Laughlin MH
    We tested the hypothesis that physical activity can attenuate the temporal decline of acetylcholine-induced endothelium dependent relaxation during type 2 diabetes mellitus progression in the Otsuka Long-Evans Tokushima Fatty (OLETF) rat. OLETF sedentary rats exhibited decreased acetylcholine-induced abdominal aortic endothelium dependent relaxation from 13 weeks of age (wk) to 20wk (20-35%) and from 13wk to 40wk (35-50%). Acetylcholine-induced endothelium dependent relaxation was maintained in the OLETF physically active and the control sedentary Long-Evans Tokushima Otsuka (LETO) groups from 13wk to 40wk. Aortic pre-treatment with N(G)-nitro-L-arginine (LN), indomethacin (INDO), and LN+INDO did not alter...</description>
            <author>Am J Physiol Heart C...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3395448</comments>
            <pubDate>Fri, 19 Mar 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3395448</guid>        </item>
        <item>
            <title>Roles for Nox4 in the Contractile Response of Bovine Pulmonary Arteries to Hypoxia.</title>
            <link>http://www.medworm.com/index.php?rid=3395447&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%3D20304813%26dopt%3DAbstract</link>
            <description>This study examines the roles of BPA Nox oxidases and mitochondria in the HPV response. Inhibitors of Nox2 (0.1mM apocynin and 50muM gp91-dstat) and mitochondrial electron transport (10muM antimycin and rotenone) decreased superoxide generation in BPA without affecting contraction to 25mM KCl or the HPV response. Transfection of BPA with siRNA for Nox2 and Nox4 decreased Nox2 and Nox4 protein expression, respectively, associated with an attenuation of superoxide detection, without affecting 25mM KCl contraction. However, Nox4 siRNA, but, not Nox2 attenuated HPV in BPA. A Nox4 inhibitor plumbagin (10muM) increased basal force, decreased superoxide detection and peroxide release, and caused BPA to relax under hypoxia. While acute removal of peroxide with 0.1mM ebselen increased 25mM KCl cont...</description>
            <author>Am J Physiol Heart C...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3395447</comments>
            <pubDate>Fri, 19 Mar 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3395447</guid>        </item>
        <item>
            <title>Role of Ca2+/calmodulin-dependent protein kinase II in the regulation of the cardiac L-type Ca2+ current during endothelin-1 stimulation.</title>
            <link>http://www.medworm.com/index.php?rid=3395446&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%3D20304814%26dopt%3DAbstract</link>
            <description>Authors: Komukai K, O-Uchi J, Morimoto S, Kawai M, Hongo K, Yoshimura M, Kurihara S
    Endothelin-1 (ET-1) shows a positive inotropic effect on cardiac muscle. Although the L-type Ca(2+) current (ICa) is one of the important determinants of cardiac excitation-contraction coupling, the effect of ET-1 on the ICa is not always clear. The controversial results appear to be due to different patch clamp methods. The present study measured the effect of ET-1 on the ICa of rat ventricular myocytes using the perforated patch clamp technique. The holding potential was set -40 mV and depolarization was applied every 10 s. ET-1 (10 nM) increased the ICa in a monophasic manner. The current reached a steady state 15 min after the application of ET-1, when the measurement was done. Endothelin receptor s...</description>
            <author>Am J Physiol Heart C...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3395446</comments>
            <pubDate>Fri, 19 Mar 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3395446</guid>        </item>
        <item>
            <title>MnSOD protects against COX1-mediated endothelial dysfunction in chronic heart failure.</title>
            <link>http://www.medworm.com/index.php?rid=3395445&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%3D20304815%26dopt%3DAbstract</link>
            <description>Authors: Miller JD, Peotta VA, Chu Y, Weiss RM, Zimmerman KA, Brooks RM, Heistad DD
    Endothelial function is impaired by oxidative stress in chronic heart failure (HF). Mechanisms that protect against increases in oxidative stress in HF are not clear. The goal of this study was to determine whether manganese superoxide dismutase (MnSOD) plays a key role in protecting against endothelial dysfunction in HF. Endothelial function and gene expression were examined in aorta from wild-type mice (MnSOD(+/+)) and mice deficient in manganese superoxide dismutase (MnSOD(+/-)) 12 weeks after ligation of the left coronary artery (LCA). LCA ligation produced similar size myocardial infarctions in MnSOD(+/+) and MnSOD(+/-) mice, and reduced ejection fraction to ~20% in both groups. Maximal relaxation ...</description>
            <author>Am J Physiol Heart C...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3395445</comments>
            <pubDate>Fri, 19 Mar 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3395445</guid>        </item>
        <item>
            <title>Isoform- and tissue-specific regulation of the Ca2+-sensitive transcription factor NFAT in cardiac myocytes and in heart failure.</title>
            <link>http://www.medworm.com/index.php?rid=3395444&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%3D20304816%26dopt%3DAbstract</link>
            <description>This study compared basal localization, import and export of NFATc1 and NFATc3 in adult atrial and ventricular myocytes to identify isoform- and tissue-specific regulatory mechanisms of NFAT activation under physiological conditions and in heart failure. NFAT-GFP fusion proteins and NFAT immunocytochemistry were used to analyze NFAT regulation in adult cat and rabbit myocytes. NFATc1 displayed basal nuclear localization in atrial and ventricular myocytes, an effect that was reversed by reducing [Ca(2+)]i and inhibiting CaN, and enhanced by inhibition of nuclear export. In contrast NFATc3 was localized to the cytoplasm, but could be driven to the nucleus by angiotensin II and endothelin-1 stimulation in atrial, but not ventricular cells. Inhibition of nuclear export (by Leptomycin B) facili...</description>
            <author>Am J Physiol Heart C...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3395444</comments>
            <pubDate>Fri, 19 Mar 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3395444</guid>        </item>
        <item>
            <title>Cardiac oxidative stress is involved in heart failure induced by thiamine deprivation in rats.</title>
            <link>http://www.medworm.com/index.php?rid=3395443&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%3D20304817%26dopt%3DAbstract</link>
            <description>Authors: Gioda CR, de Oliveira Barreto T, Gomes TN, de Lima D, Campos PP, Capettini LS, Lauton-Santos S, Vasconcelos A, Coimbra CC, Lemos VS, Pesquero JL, Cruz JS
    Thiamine is an important cofactor of metabolic enzymes, and its deficiency leads to cardiovascular dysfunction. Firstly we characterized the metabolic status measuring resting oxygen consumption rate and lactate blood concentration after 35 days of thiamine deficiency. The results pointed to a decrease in resting oxygen consumption and a two-fold increase in blood lactate. Confocal microscopy showed that intracellular superoxide (approximately 40%) and H2O2 (2.5 times) contents had been increased. In addition, biochemical activities and protein expression of superoxide-dismutase, glutathione-peroxidase and catalase were evalu...</description>
            <author>Am J Physiol Heart C...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3395443</comments>
            <pubDate>Fri, 19 Mar 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3395443</guid>        </item>
        <item>
            <title>Adrenal GRK2 lowering is an underlying mechanism for the beneficial sympathetic effects of exercise training in heart failure.</title>
            <link>http://www.medworm.com/index.php?rid=3395442&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%3D20304818%26dopt%3DAbstract</link>
            <description>Authors: Rengo G, Leosco D, Zincarelli C, Marchese M, Corbi G, Liccardo D, Filippelli A, Ferrara N, Lisanti MP, Koch WJ, Lymperopoulos A
    Exercise training has been reported to exert beneficial effects on cardiac function and to reduce morbidity and mortality of chronic heart failure (HF). Augmented sympathetic nervous system (SNS) activity, leading to elevated circulating catecholamine (CA) levels, is a hallmark of chronic HF that significantly aggravates this disease. Exercise training has been shown to also reduce SNS overactivity in HF but the underlying molecular mechanism(s) remain unidentified. We recently reported that adrenal G-protein coupled receptor kinase-2 (GRK2), an enzyme that regulates the sympatho-inhibitory alpha2-adrenoceptors (alpha2-ARs) present in the CA-producing...</description>
            <author>Am J Physiol Heart C...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3395442</comments>
            <pubDate>Fri, 19 Mar 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3395442</guid>        </item>
        <item>
            <title>Developmental Aspects of Cardiac Ca2+ Signaling: Interplay Between RyR and IP3R gated Ca2+ Stores.</title>
            <link>http://www.medworm.com/index.php?rid=3395441&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%3D20304819%26dopt%3DAbstract</link>
            <description>Authors: Janowski E, Berrios M, Cleemann L, Morad M
    The dominant mode of intracellular Ca(2+)-release in adult mammalian heart is gated by ryanodine receptors (RyRs), but it is less clear if IP3-gated Ca(2+) release channels (IP3Rs), that are important during embryogenesis, play a significant role during early post-natal development. To address this question, we measured confocal 2-D Ca(2+)-dependent fluorescence images (Fluo-4) in acutely isolated neonatal (day 1-2 ) and juvenile (day 8-10) rat cardiomyocytes, either voltage-clamped or permeabilized, where rapid exchange of solution could be used to selectively activate the two types of Ca(2+) release channel. Targeting RyRs with caffeine produced large and rapid Ca(2+) signals throughout the cells. Application of ATP and endothelin-1...</description>
            <author>Am J Physiol Heart C...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3395441</comments>
            <pubDate>Fri, 19 Mar 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3395441</guid>        </item>
        <item>
            <title>The p75 neurotrophin receptor, semaphorins and sympathetic traffic in the heart.</title>
            <link>http://www.medworm.com/index.php?rid=3395440&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%3D20304820%26dopt%3DAbstract</link>
            <description>Authors: Carter BD, Feng N, Paolocci N
    n/a Key words: p75NTR, semaphorins, nerve growth factor, sympathetic fibers.
    PMID: 20304820 [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=3395440</comments>
            <pubDate>Fri, 19 Mar 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3395440</guid>        </item>
        <item>
            <title>Measurements of changes in left ventricular volume, strain, and twist during isovolumic relaxation using MRI.</title>
            <link>http://www.medworm.com/index.php?rid=3395439&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%3D20304821%26dopt%3DAbstract</link>
            <description>In conclusion, LV relaxation during IVR is associated with changes in principal strains and untwisting, which are all correlated with an apparent increase in LV volume. Since closed mitral and aortic valves ensure true isovolumic conditions, the apparent volume change likely reflects expansion of the LV myocardium and the inward bowing of the closed mitral leaflets toward the LV interior. Key words: diastolic function, active relaxation, mitral valve leaflets.
    PMID: 20304821 [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=3395439</comments>
            <pubDate>Fri, 19 Mar 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3395439</guid>        </item>
        <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>
            <guid isPermaLink="false">3288433</guid>        </item>
        <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>Letter to the editor: &quot;Postulated functional advantages of a looped as opposed to a linearly arranged heart&quot;.
    Am J Physiol Heart Circ Physiol. 2010 Feb;298(2):H726; author reply H727
    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>Letter to the editor: &quot;Depolarization and repolarization alternans in an anesthetized canine ischemia model&quot;.
    Am J Physiol Heart Circ Physiol. 2010 Feb;298(2):H728; author reply H729
    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>
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