Cardiovascular ToxicologyThis is an RSS file. You can use it to subscribe to this data in your favourite RSS reader, such as GoogleReader, or to display this data on your own website or blog. Subscribe to this data using MyMedWorm.Subscribe to this data using GoogleReader.Subscribe to this data using Bloglines.Subscribe to this data using MyYahoo.

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136 records returned

Erratum to: Antiarrhythmic Effects of Some Antioxidant Vitamins in Rats Injected with Epinephrine.Email this article to a colleague. Save this article to My Clippings. Discuss or comment on this article.
PMID: 19924570 [PubMed - as supplied by publisher] (Source: Cardiovascular Toxicology)
Source: Cardiovascular Toxicology - November 19, 2009 Category: Cardiology Authors: Sethi R, Rehsia NS, Jindal K, Dhalla KS, Elimban V, Dhalla NS Tags: Cardiovasc Toxicol Source Type: journals

Mechanisms of Myocyte Cytotoxicity Induced by the Multikinase Inhibitor Sorafenib.Email this article to a colleague. Save this article to My Clippings. Discuss or comment on this article.
In conclusion, given the extreme lack of kinase selectivity that sorafenib exhibits, it is likely that inhibition of kinases other than RAF, or combinations of kinases, contributes to the cardiotoxic effects of sorafenib. PMID: 19915982 [PubMed - as supplied by publisher] (Source: Cardiovascular Toxicology)
Source: Cardiovascular Toxicology - November 14, 2009 Category: Cardiology Authors: Hasinoff BB, Patel D Tags: Cardiovasc Toxicol Source Type: journals

Erythropoietin Promotes Deleterious Cardiovascular Effects and Mortality Risk in a Rat Model of Chronic Sports Doping.Email this article to a colleague. Save this article to My Clippings. Discuss or comment on this article.
In conclusion, rhEPO doping in rats under chronic exercise promotes not only the expected RBC count increment, suggesting hyperviscosity, but also other serious deleterious cardiovascular and thromboembolic modifications, including mortality risk, which might be known and assumed by all sports authorities, including athletes and their physicians. PMID: 19859831 [PubMed - as supplied by publisher] (Source: Cardiovascular Toxicology)
Source: Cardiovascular Toxicology - October 27, 2009 Category: Cardiology Authors: Piloto N, Teixeira HM, Teixeira-Lemos E, Parada B, Garrido P, Sereno J, Pinto R, Carvalho L, Costa E, Belo L, Santos-Silva A, Teixeira F, Reis F Tags: Cardiovasc Toxicol Source Type: journals

Mitochondrial Involvement in Cardiac Apoptosis During Ischemia and Reperfusion: Can We Close the Box?Email this article to a colleague. Save this article to My Clippings. Discuss or comment on this article.
Myocardial ischemia is the main cause of death in the Western societies. Therapeutic strategies aimed to protect the ischemic myocardium have been extensively studied. Reperfusion is the definitive treatment for acute coronary syndromes, especially acute myocardial infarction; however, reperfusion has the potential to exacerbate tissue injury, a process termed reperfusion injury. Ischemia/reperfusion (I/R) injury may lead to cardiac arrhythmias and contractile dysfunction that involve apoptosis and necrosis in the heart. The present review describes the mitochondrial role on cardiomyocyte death and some potential pharm...
Source: Cardiovascular Toxicology - October 24, 2009 Category: Cardiology Authors: Machado NG, Alves MG, Carvalho RA, Oliveira PJ Tags: Cardiovasc Toxicol Source Type: journals

Arsenic Exposure and Cardiovascular Disorders: An Overview.Email this article to a colleague. Save this article to My Clippings. Discuss or comment on this article.
The incidence of arsenic toxicity has been observed in various countries including Taiwan, Bangladesh, India, Argentina, Australia, Chile, China, Hungary, Peru, Thailand, Mexico and United States of America. Arsenic is a ubiquitous element present in drinking water, and its exposure is associated with various cardiovascular disorders. Arsenic exposure plays a key role in the pathogenesis of vascular endothelial dysfunction as it inactivates endothelial nitric oxide synthase, leading to reduction in the generation and bioavailability of nitric oxide. In addition, the chronic arsenic exposure induces high oxidative stres...
Source: Cardiovascular Toxicology - September 28, 2009 Category: Cardiology Authors: Balakumar P, Kaur J Tags: Cardiovasc Toxicol Source Type: journals

An Elementary Framework for Judging the Cardiovascular Toxicity of Carbon Soot: Experiences from an Occupational Health Survey of Diamond Industry Workers.Email this article to a colleague. Save this article to My Clippings. Discuss or comment on this article.
The objective of this study is to assess the cardiovascular effects consequent to chronic respiratory exposure of carbon soot. A cross-sectional occupational health survey was conducted in all consenting workers who employed in the production wing of diamond-processing industries. Blood pressure, ECGs, height, weight, and blood counts were measured and evaluated. Blood pressure measurements revealed a high prevalence of hypertension in young workers. Left atrial abnormality (LAA) was the major finding in the electrocardiograms. We found a high prevalence of hypertension in young diamond workers. The LASER saw operators had...
Source: Cardiovascular Toxicology - September 23, 2009 Category: Cardiology Authors: Beniwal R, Shivgotra VK Tags: Cardiovasc Toxicol Source Type: journals

Mitochondrial Preservation in Celsior Versus Histidine Buffer Solution During Cardiac Ischemia and Reperfusion.Email this article to a colleague. Save this article to My Clippings. Discuss or comment on this article.
Various stressful conditions such as ischemia in cold cardioplegic solutions and reperfusion occur during heart transplantation. Since ATP production is essential for the maintenance of contractile activity, mitochondrial function may be a mediator of ischemia and ischemia/reperfusion (I/R) injury. We aimed at testing the ability of two distinct cardioplegic solutions, Celsior (Cs) and Histidine Buffer (HBS), to protect rat heart mitochondria (HM) function during ischemia alone or ischemia followed by reperfusion. A standard Krebs-Henseleit solution (KH) was used as "negative" control. Male and Female Wistar rats were ...
Source: Cardiovascular Toxicology - September 14, 2009 Category: Cardiology Authors: Alves MG, Oliveira PJ, Carvalho RA Tags: Cardiovasc Toxicol Source Type: journals

Preventive Effect of Amiodarone During Acute Period in Isoproterenol-Induced Myocardial Injury in Wistar Rats.Email this article to a colleague. Save this article to My Clippings. Discuss or comment on this article.
The ability of amiodarone to prevent pathological changes and oxidative stress after isoproterenol (ISO)-induced myocardial injury was investigated in rats. A better understanding of the processes involved in the pathophysiology of myocardial infarction has led to the search for drugs that can limit the extent of myocardial injury. Amiodarone was administered to groups of rats groups once per day for 30 days. On days 29 and 30, the rats of the ISO control and drug treatment groups were administered 180 mg/kg ISO subcutaneously at an interval of 24 h for two consecutive days. In the control groups, clinical indicators, ...
Source: Cardiovascular Toxicology - August 27, 2009 Category: Cardiology Authors: Albayrak F, Bayir Y, Halici Z, Kabalar E, Bayram E, Ozturk C, Suleyman H, Keles MS, Kurt M, Bakan E Tags: Cardiovasc Toxicol Source Type: journals

P38 MAP Kinase Inhibitor Prevents Diastolic Dysfunction in Rats Following HIV gp120 Injection In vivo.Email this article to a colleague. Save this article to My Clippings. Discuss or comment on this article.
HIV infection in patients is associated with a surprisingly high frequency of diastolic dysfunction followed by the development of a dilated cardiomyopathy. Potential mechanisms include direct effects of HIV proteins, including gp120. We have previously reported direct inotropic and p38 MAP kinase signaling effects of HIV gp120 on isolated cardiac myocytes in vitro. We now report effects of a single injection of HIV gp120 on cardiac hemodynamics in vivo. HIV gp120 (50 mug/kg) was injected intravenously and hemodynamics assessed at 1, 24, 48 and 72 h in freely ambulatory, awake rats. Rats injected with gp120 demonstrate...
Source: Cardiovascular Toxicology - July 30, 2009 Category: Cardiology Authors: Berzingi C, Chen F, Finkel MS Tags: Cardiovasc Toxicol Source Type: journals

Zinc Antagonizes Homocysteine-Induced Fetal Heart Defects in Rats.Email this article to a colleague. Save this article to My Clippings. Discuss or comment on this article.
It has been suggested that zinc may have a protective role against heart defects during fetal development. We investigated the effects of zinc on the development of fetal cardiac malformations induced by homocysteine. Pregnant Sprague-Dawley rats were randomized into one of five groups: control (C), homocysteine (H), homocysteine + zinc (Z), homocysteine + folic acid (F), or homocysteine + zinc + folic acid (ZF) (each n = 8). Homocysteine (8 nmol/day) was administered intraperitoneally in the H, Z, F, and ZF groups on gestation days (GD) 8, 9, and 10. Zinc (30 mg/kg day), folic acid (30 mg/kg day), or both (30 mg/kg da...
Source: Cardiovascular Toxicology - July 29, 2009 Category: Cardiology Authors: He X, Hong X, Zeng F, Kang F, Li L, Sun Q Tags: Cardiovasc Toxicol Source Type: journals

Dose Dependency and Reversibility of Serotonin-Induced Valvular Heart Disease in Rats.Email this article to a colleague. Save this article to My Clippings. Discuss or comment on this article.
In conclusion, this study provides evidence for a dose-dependent valvular toxicity of serotonergic drugs, which appears to be reversible after drug withdrawal. PMID: 19609730 [PubMed - as supplied by publisher] (Source: Cardiovascular Toxicology)
Source: Cardiovascular Toxicology - July 15, 2009 Category: Cardiology Authors: Droogmans S, Roosens B, Cosyns B, Degaillier C, Hernot S, Weytjens C, Garbar C, Caveliers V, Pipeleers-Marichal M, Franken PR, Bossuyt A, Schoors D, Lahoutte T, Van Camp G Tags: Cardiovasc Toxicol Source Type: journals

Report and Recommendations of the Workshop of the European Centre for the Validation of Alternative Methods for Drug-Induced Cardiotoxicity.Email this article to a colleague. Save this article to My Clippings. Discuss or comment on this article.
Cardiotoxicity is among the leading reasons for drug attrition and is therefore a core subject in non-clinical and clinical safety testing of new drugs. European Centre for the Validation of Alternative Methods held in March 2008 a workshop on "Alternative Methods for Drug-induced Cardiotoxicity" in order to promote acceptance of alternative methods reducing, refining or replacing the use of laboratory animals in this field. This review reports the outcome of the workshop. The participants identified the major clinical manifestations, which are sensitive to conventional drugs, to be arrhythmias, contractility toxicity,...
Source: Cardiovascular Toxicology - July 1, 2009 Category: Cardiology Authors: Stummann TC, Beilmann M, Duker G, Dumotier B, Fredriksson JM, Jones RL, Hasiwa M, Kang YJ, Mandenius CF, Meyer T, Minotti G, Valentin YJ, Zünkler BJ, Bremer S Tags: Cardiovasc Toxicol Source Type: journals

Comparison of the Cardiac Electrophysiology and General Toxicology of Two Formulations of Intravenous Amiodarone in Dogs.Email this article to a colleague. Save this article to My Clippings. Discuss or comment on this article.
Intravenous amiodarone (AIV) must be administered slowly after dilution to avoid hypotension, which is due to the cosolvents polysorbate 80 and benzyl alcohol used in its formulation. PM101 is a formulation of amiodarone devoid of these cosolvents, which enables bolus administration. We evaluated any potential toxicity or exaggerated adverse cardiac electrophysiologic effects of PM101 compared with AIV and control. Beagle dogs were treated with the human-equivalent amiodarone loading dose (2.14 mg/kg) with PM101 (bolus push) or AIV (10 min infusion in the toxicology study and bolus push in the electrophysiology study) ...
Source: Cardiovascular Toxicology - June 24, 2009 Category: Cardiology Authors: Cushing DJ, Cooper WD, Gralinski MR, Lipicky RJ, Kudenchuk PJ, Kowey PR Tags: Cardiovasc Toxicol Source Type: journals

ST elevation myocardial infarction presenting after use of pseudoephedrine.Email this article to a colleague. Save this article to My Clippings. Discuss or comment on this article.
PMID: 19381878 [PubMed - in process] (Source: Cardiovascular Toxicology)
Source: Cardiovascular Toxicology - May 31, 2009 Category: Cardiology Authors: Celik A Tags: Cardiovasc Toxicol Source Type: journals

Influence of infrasound exposure on the whole L-type calcium currents in rat ventricular myocytes.Email this article to a colleague. Save this article to My Clippings. Discuss or comment on this article.
This study was designed to examine the effect of infrasound exposure (5 Hz at 130 dB) on whole-cell L-type Ca2+ currents (WLCC) in rat ventricular myocytes and the underlying mechanism(s) involved. Thirty-two adult Sprague-Dawley rats were randomly assigned to infrasound exposure and control groups. [Ca2+](i), WLCC, mRNA expression of the a(1c) subunit of L-type Ca2+ channels (LCC), and SERCA2 protein were examined on day 1, 7, and 14 after initiation of infrasound exposure. Fluo-3/AM fluorescence and the laser scanning confocal microscope techniques were used to measure [Ca2+](i) in freshly isolated ventricular myocytes. ...
Source: Cardiovascular Toxicology - May 31, 2009 Category: Cardiology Authors: Pei Z, Zhuang Z, Xiao P, Chen J, Sang H, Ren J, Wu Z, Yan G Tags: Cardiovasc Toxicol Source Type: journals

The cardiac effects of prolonged vitamin B12 and folate deficiency in rats.Email this article to a colleague. Save this article to My Clippings. Discuss or comment on this article.
In the recent past, hyperhomocysteinemia (HHCY) has been linked to chronic heart failure. Folate and vitamin B12 deficiencies are the common causes of HHCY. The impact of these vitamins on cardiac function and morphology has scarcely been investigated. The aim of this study was to conduct an analysis of the cardiac effect of folate and vitamin B12 deficiency in vivo. Two groups of rats, a control (Co, n = 10) and a vitamin-deficient group (VitDef, n = 10), were fed for 12 weeks with a folate and vitamin B12-free diet or an equicaloric control diet. Plasma and tissue concentrations of HCY, S-adenosyl-homocysteine (SAH),...
Source: Cardiovascular Toxicology - May 31, 2009 Category: Cardiology Authors: Taban-Shomal O, Kilter H, Wagner A, Schorr H, Umanskaya N, Hübner U, Böhm M, Herrmann W, Herrmann M Tags: Cardiovasc Toxicol Source Type: journals

Commentary on "A case of acute cardiomyopathy and pericarditis associated with methylphenidate"; Cardiovasc Toxicol, DOI 10.1007/s12012-009-9033-7.Email this article to a colleague. Save this article to My Clippings. Discuss or comment on this article.
PMID: 19415530 [PubMed - in process] (Source: Cardiovascular Toxicology)
Source: Cardiovascular Toxicology - May 31, 2009 Category: Cardiology Authors: Ghanizadeh A Tags: Cardiovasc Toxicol Source Type: journals

Quo vadis: whither homocysteine research?Email this article to a colleague. Save this article to My Clippings. Discuss or comment on this article.
Four decades of research on the link between hyperhomocysteinemia and cardiovascular disease has led to a crossroads. Several negative studies on the role of homocysteine-lowering B-vitamin therapy in reducing the risk of atherothrombotic cardiovascular disease have dampened enthusiasm for this important field of research. In this review, we assess the present state of homocysteine research and suggest potential avenues that would help to clarify the purported link between the plasma homocysteine level and cardiovascular risk. We address several questions raised by the findings of various basic, epidemiological and cli...
Source: Cardiovascular Toxicology - May 31, 2009 Category: Cardiology Authors: Joseph J, Handy DE, Loscalzo J Tags: Cardiovasc Toxicol Source Type: journals

Cardiac lesions induced by testosterone: protective effects of dexrazoxane and trimetazidine.Email this article to a colleague. Save this article to My Clippings. Discuss or comment on this article.
Further to our previous observation of post-mortem cardiac lesions after sudden death in several athletes with a history of anabolic steroid abuse, this study was intended to reproduce these lesions in rabbits administered testosterone oenanthate, a prototypic anabolic steroid abused by athletes, and to provide evidence for the protective effects of trimetazidine and dexrazoxane that are used as antianginal and cardioprotective drugs, respectively. Groups of six rabbits each were administered saline, testosterone, or a combination of testosterone and either trimetazidine or dexrazoxane for 3 months. Histologic cardiac ...
Source: Cardiovascular Toxicology - May 31, 2009 Category: Cardiology Authors: Belhani D, Fanton L, Vaillant F, Descotes J, Manati W, Tabib A, Bui-Xuan B, Timour Q Tags: Cardiovasc Toxicol Source Type: journals

AZT-induced oxidative cardiovascular toxicity: attenuation by Mg-supplementation.Email this article to a colleague. Save this article to My Clippings. Discuss or comment on this article.
Cardiovascular effects of chronic AZT treatment on SD male rats (185 g) fed either a normal Mg diet (0.1% MgO) or a high Mg diet (0.6% MgO) were examined. AZT treatment (1 mg/ml drinking water) for 3 weeks led to a 5.5-fold (0.88 +/- 0.11 nmol/min/10(6) cells, P < 0.05) elevation in neutrophil basal activity of O2(-) production versus controls (0.16 +/- 0.03 nmol/min, assayed ex vivo as SOD-inhibitable cytochrome c reduction). Concomitantly, plasma 8-isoprostane and PGE(2) levels rose 2.1-fold and 3-fold (both P < 0.05), respectively, compared to control; however, RBC GSH decreased 28% (P < 0.02) with GSSG con...
Source: Cardiovascular Toxicology - May 31, 2009 Category: Cardiology Authors: Mak IT, Chmielinska JJ, Kramer JH, Weglicki WB Tags: Cardiovasc Toxicol Source Type: journals

Zinc- and copper-induced interleukin-6 release in primary cell cultures from rat heart.Email this article to a colleague. Save this article to My Clippings. Discuss or comment on this article.
In conclusion, Zn2+ and Cu2+ increased IL-6 release and MAP-kinase activation in primary cardiac cells, processes known to be involved in cardiac inflammation and hypertrophy. PMID: 19517273 [PubMed - in process] (Source: Cardiovascular Toxicology)
Source: Cardiovascular Toxicology - May 31, 2009 Category: Cardiology Authors: Ansteinsson V, Refsnes M, Skomedal T, Osnes JB, Schiander I, Låg M Tags: Cardiovasc Toxicol Source Type: journals

Dilated Cardiomyopathy in Transgenic Mice Expressing HIV Tat.Email this article to a colleague. Save this article to My Clippings. Discuss or comment on this article.
Mechanisms responsible for HIV cardiomyopathy are unknown, but may include direct effects of HIV proteins on the heart. Transgenic mice (TG) expressing HIV Tat protein targeted to the myocardium, +/- Tat TG, have revealed anatomical and biochemical defects in the heart. The present studies were conducted to clarify the effect of Tat on cardiac function. In vivo hemodynamics was measured in awake mice after inserting a catheter tip in the left ventricle under general anesthesia. Under the age of 3 months, the heart rate (HR) was significantly lower in TG (591 +/- 47 vs. 716 +/- 45 bpm, TG versus FVB control (FVB), respe...
Source: Cardiovascular Toxicology - April 1, 2009 Category: Cardiology Authors: Fang Q, Kan H, Lewis W, Chen F, Sharma P, Finkel MS Tags: Cardiovasc Toxicol Source Type: journals

Metabolites of MDMA Induce Oxidative Stress and Contractile Dysfunction in Adult Rat Left Ventricular Myocytes.Email this article to a colleague. Save this article to My Clippings. Discuss or comment on this article.
In this study, we demonstrated that metabolites of MDMA induce oxidative stress and contractile dysfunction in adult rat left ventricular myocytes. Metabolites of MDMA used in this study included alpha-methyl dopamine, N-methyl alpha-methyl dopamine and 2,5-bis(glutathion-S-yl)-alpha-MeDA. Dihydroethidium was used to detect drug-induced increases in reactive oxygen species (ROS) production in ventricular myocytes. Contractile function and changes in intracellular calcium transients were measured in paced (1 Hz), Fura-2 AM loaded, myocytes using the IonOptix system. Production of ROS in ventricular myocytes treated with MDM...
Source: Cardiovascular Toxicology - March 31, 2009 Category: Cardiology Authors: Shenouda SK, Varner KJ, Carvalho F, Lucchesi PA Tags: Cardiovasc Toxicol Source Type: journals

A Case of Acute Cardiomyopathy and Pericarditis Associated with Methylphenidate.Email this article to a colleague. Save this article to My Clippings. Discuss or comment on this article.
We report the case of a 17-year-old male who developed chest pain, elevated cardiac biomarkers, and acute left ventricular dysfunction following a single dose of methylphenidate. The risk of cardiomyopathy in the setting of methylphenidate treatment should prompt further study on the safety of this drug, and lead to ways of identifying those at risk of developing these complications. PMID: 19296063 [PubMed - as supplied by publisher] (Source: Cardiovascular Toxicology)
Source: Cardiovascular Toxicology - March 19, 2009 Category: Cardiology Authors: Dadfarmay S, Dixon J Tags: Cardiovasc Toxicol Source Type: journals

Acute Myocardial Infarction Following Oral Methyl-Ergometrine Intake.Email this article to a colleague. Save this article to My Clippings. Discuss or comment on this article.
We report the case of a 38-year-old woman with a ST elevation myocardial infarction (STEMI) few days after artificially induced abortion by oral prescription of methylergometrine. Coronary angiography performed 2 days after onset of chest pain did not reveal any abnormalities of the coronary arteries but a provocative test using intravenous methylergometrine was positive with reproduction of chest pain, ECG changes and with a significant narrowing localized on the second segment of the left anterior descending artery at the angiogram. Thus, since methylergometrin may clearly induce coronary spasm when prescribed orally, ch...
Source: Cardiovascular Toxicology - February 14, 2009 Category: Cardiology Authors: de Labriolle A, Genée O, Heggs LM, Fauchier L Tags: Cardiovasc Toxicol Source Type: journals

Expression of Nkx2.5 in Wild Type, Cardiac Mutant, and Thyroxine-Induced Metamorphosed Hearts of the Mexican Axolotl.Email this article to a colleague. Save this article to My Clippings. Discuss or comment on this article.
In this study, we cloned and sequenced the as yet uncharacterized Nkx2.5 cDNA from normal and cardiac mutant axolotl heart RNA. Comparison of cDNA sequences of Nkx2.5 from normal and mutant axolotl hearts did not show differences suggesting that loss of function mutation in Nkx2.5 is not responsible for the mutant phenotype. However, quantitative studies show higher expression of Nkx2.5 in mutant hearts raising the possibility that increased expression of Nkx2.5 may contribute to the mutant phenotype. We also evaluated quantitative changes in expression of Nkx2.5 in axolotl hearts during embryonic and postembryonic heart d...
Source: Cardiovascular Toxicology - February 4, 2009 Category: Cardiology Authors: Thurston HL, Prayaga S, Thomas A, Guharoy V, Dube S, Poiesz BJ, Dube DK Tags: Cardiovasc Toxicol Source Type: journals

Long-Term Exposure to AZT, but not d4T, Increases Endothelial Cell Oxidative Stress and Mitochondrial Dysfunction.Email this article to a colleague. Save this article to My Clippings. Discuss or comment on this article.
Nucleoside reverse transcriptase inhibitors (NRTIs), such as zidovudine (AZT) and stavudine (d4T), cause toxicities to numerous tissues, including the liver and vasculature. While much is known about hepatic NRTI toxicity, the mechanism of toxicity in endothelial cells is incompletely understood. Human aortic endothelial and HepG2 liver cells were exposed to 1 muM AZT or d4T for up to 5 weeks. Markers of oxidative stress, mitochondrial function, NRTI phosphorylation, mitochondrial DNA (mtDNA) levels, and cytotoxicity were monitored over time. In endothelial cells, AZT significantly oxidized glutathione redox potential,...
Source: Cardiovascular Toxicology - December 9, 2008 Category: Cardiology Authors: Kline ER, Bassit L, Hernandez-Santiago BI, Detorio MA, Liang B, Kleinhenz DJ, Walp ER, Dikalov S, Jones DP, Schinazi RF, Sutliff RL Tags: Cardiovasc Toxicol Source Type: journals

A Hyperlipidemic Rabbit Model Provides New Insights into Pulmonary Zinc Exposure Effects on Cardiovascular Health.Email this article to a colleague. Save this article to My Clippings. Discuss or comment on this article.
This study ascertains the effects of zinc, a major component of particulate matter, on pulmonary and systemic endpoints using hyperlipidemic rabbits to model diet-induced human atherosclerosis. New Zealand White rabbits were fed a normal or cholesterol-enriched diet and then were intratracheally instilled 1x/week for 4 weeks with saline or 16 microg/kg of zinc, equal parts sulfate and oxide. Physiologic responses, blood after each exposure, and terminal bronchoalveolar lavage (BAL) were assessed. Rabbits fed a cholesterol-rich diet developed hyperlipidemia and had consistently higher circulating leukocyte counts than rabbi...
Source: Cardiovascular Toxicology - October 25, 2008 Category: Cardiology Authors: Lagier AJ, Manzo ND, Carll AP, Jaskot RH, Slade R, Richards JH, Winsett DW, Farraj AK, Dye JA Tags: Cardiovasc Toxicol Source Type: journals

Hypertension, Cardiac Hypertrophy, and Impaired Vascular Relaxation Induced by 2,3,7,8-Tetrachlorodibenzo-p-Dioxin are Associated with Increased Superoxide.Email this article to a colleague. Save this article to My Clippings. Discuss or comment on this article.
The mechanisms by which 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) increases the incidence of human cardiovascular disease are not known. We investigated the degree to which cardiovascular disease develops in mice following subchronic TCDD exposure. Adult male C57BL/6 mice were dosed with vehicle or 300 ng TCDD/kg by oral gavage three times per week for 60 days. Blood pressure was recorded by radiotelemetry and aortic endothelial function was assessed by acetylcholine-induced vasorelaxation. Mean arterial pressure of TCDD-exposed mice was increased significantly by day 4 and between days 7-10, 25-35, and 45-60 with two...
Source: Cardiovascular Toxicology - October 11, 2008 Category: Cardiology Authors: Kopf PG, Huwe JK, Walker MK Tags: Cardiovasc Toxicol Source Type: journals

CXCR4 Receptor Antagonist Blocks Cardiac Myocyte P38 MAP Kinase Phosphorylation by HIV gp120.Email this article to a colleague. Save this article to My Clippings. Discuss or comment on this article.
The prognosis for patients with human immunodeficiency virus (HIV) infection has improved remarkably as a result of effective antiretroviral therapy. This has resulted in an increased awareness of cardiac complications from HIV infection, including cardiomyopathy and overt heart failure. Mechanisms responsible for HIV cardiomyopathy and heart failure are unknown, but may include direct effects of HIV proteins on the heart. We have previously reported that the HIV envelope glycoprotein, gp120, has a p38 MAP kinase-dependent negative inotropic effect on adult rat ventricular myocytes (ARVM). This signaling pathway presum...
Source: Cardiovascular Toxicology - October 11, 2008 Category: Cardiology Authors: Yuan Y, Kan H, Fang Q, Chen F, Finkel MS Tags: Cardiovasc Toxicol Source Type: journals

Molecular Analysis of Cocaine-Induced Endothelial Dysfunction: Role of Endothelin-1 and Nitric Oxide.Email this article to a colleague. Save this article to My Clippings. Discuss or comment on this article.
Cocaine remains the most frequently used illicit substance. Although cocaine-induced atherosclerosis is well documented, its mechanism of action on human vascular endothelial cells has not been determined. Nitric oxide (NO) and endothelin-1 (ET-1) are involved in endothelial cell activation and leukocyte recruitment. The present study monitored the effects of cocaine on NO and ET-1 production in human aortic endothelial cells (HAECs) and the effects of sodium nitroprusside (SNP) and BQ-123 on leukocyte adhesion to HAECs. Acute exposure to cocaine (1 and 3 muM) significantly increased ET-1 production (2-fold) and ET-1 r...
Source: Cardiovascular Toxicology - September 24, 2008 Category: Cardiology Authors: Pradhan L, Mondal D, Chandra S, Ali M, Agrawal KC Tags: Cardiovasc Toxicol Source Type: journals

The Prevalence of Type 2 Diabetes and Hypertension in Uygur and Kazak Populations.Email this article to a colleague. Save this article to My Clippings. Discuss or comment on this article.
This study was designed to evaluate the epidemiology of type 2 diabetes and hypertension in Uygur and Kazak ethnic populations. A three-step stratified sampling method was used. Questionnaires, blood pressure, anthropometric measurement, and fasting blood glucose were monitored. In total, 1,571 Uygur and 2,913 Kazak subjects were randomly enrolled. The prevalence of type 2 diabetes and glucose intolerance was 5.55- and 1.90-fold higher, respectively, in Uygur than in the Kazak population (8.16 vs. 1.47%, P < 0.001 and 3.29 vs. 1.73%, P < 0.001). However, the prevalence of hypertension and obesity was significantly hi...
Source: Cardiovascular Toxicology - September 6, 2008 Category: Cardiology Authors: Tao Y, Mao X, Xie Z, Ran X, Liu X, Wang Y, Luo X, Hu M, Gen W, Zhang M, Wang T, Ren J, Wufuer H, Li L Tags: Cardiovasc Toxicol Source Type: journals

Antiplatelet Agents Sarpogrelate and Cilostazol Affect Experimentally-induced Ventricular Arrhythmias and Mortality.Email this article to a colleague. Save this article to My Clippings. Discuss or comment on this article.
Antiplatelet agents, sarpogrelate (SAR), a 5-hydroxy tryptamine 2A receptor antagonist and cilostazol (CIL), a phosphodiesterase-III inhibitor, were observed to be beneficial in attenuating cardiac remodeling and improving cardiac function in congestive heart failure due to myocardial infarction in rats; however, CIL increased ventricular tachycardia and mortality. In order to study the effects of these antiplatelet agents on arrhythmias, Sprague-Dawley rats were pretreated with either SAR or CIL (5 mg/kg/day) for 2 weeks and were then either injected cumulative doses of epinephrine (Epi) or subjected to coronary occlu...
Source: Cardiovascular Toxicology - August 27, 2008 Category: Cardiology Authors: Barta J, Sanganalmath SK, Kumamoto H, Takeda N, Edes I, Dhalla NS Tags: Cardiovasc Toxicol Source Type: journals

Estrogen-Mediated Protection in Myocardial Ischemia-Reperfusion Injury.Email this article to a colleague. Save this article to My Clippings. Discuss or comment on this article.
Before menopause, a woman has a relatively low risk for developing cardiovascular disease. After menopause, however, the risk increases nearly twofold and cardiovascular disease remains the number one cause of death among women. Observational trials and studies in animal models of cardiovascular disease suggested that females have reduced injury after myocardial ischemia and reperfusion injury. However, two large clinical trials, the women's health initiative (WHI) and the heart estrogen and progestin replacement study (HERS), found an increase in cardiovascular incidences in women taking hormone replacement therapy. T...
Source: Cardiovascular Toxicology - August 6, 2008 Category: Cardiology Authors: Booth EA, Lucchesi BR Tags: Cardiovasc Toxicol Source Type: journals

Role of Copper and Homocysteine in Pressure Overload Heart Failure.Email this article to a colleague. Save this article to My Clippings. Discuss or comment on this article.
In conclusion, our data suggest that copper supplement helps improve cardiac function in a pressure overload dilated cardiomyopathic heart. PMID: 18679830 [PubMed - as supplied by publisher] (Source: Cardiovascular Toxicology)
Source: Cardiovascular Toxicology - August 5, 2008 Category: Cardiology Authors: Hughes WM, Rodriguez WE, Rosenberger D, Chen J, Sen U, Tyagi N, Moshal KS, Vacek T, Kang YJ, Tyagi SC Tags: Cardiovasc Toxicol Source Type: journals

Perinatal 2,3,7,8-Tetrachlorodibenzo-p-dioxin Exposure Sensitizes Offspring to Angiotensin II-induced Hypertension.Email this article to a colleague. Save this article to My Clippings. Discuss or comment on this article.
In utero and lactational exposure of mice to 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) leads to cardiac hypertrophy and hydronephrosis in adulthood. We tested the hypothesis that perinatal TCDD exposure increases the susceptibility to cardiovascular disease when offspring are exposed to a common cardiovascular disease risk factor, angiotensin II (Ang II). Pregnant C57BL/6N mice were exposed to corn oil (control) or 6.0 mug/kg TCDD on gestation day 14.5. Male offspring were then exposed to a subpressor (0.1 mg/kg/day) or pressor (0.7 mg/kg/day) dose of Ang II at 3.5 months and cardiac morphology and blood pressure anal...
Source: Cardiovascular Toxicology - August 1, 2008 Category: Cardiology Authors: Aragon AC, Goens MB, Carbett E, Walker MK Tags: Cardiovasc Toxicol Source Type: journals

QT Prolongation: A Case of Arsenical Pericardial and Pleural Effusion.Email this article to a colleague. Save this article to My Clippings. Discuss or comment on this article.
We describe a case of a man, 76 years old, who was admitted to our department for dyspnoea in APL in treatment with arsenic trioxide. Chest radiograph illustrated an enlarged cardiac silhouette and bilateral pleuric effusion and the ECG evidenced QT prolongation. The patient was also submitted to transthoracic echocardiography that revealed moderate pericardial effusion without signs of cardiac tamponade and a normal biventricular function. This condition was considered to be associated with arsenic trioxide polyserosit and the drug therapy was immediately discontinued and steroid drugs started. After 2 weeks of arsenic tr...
Source: Cardiovascular Toxicology - July 16, 2008 Category: Cardiology Authors: Vizzardi E, Zanini G, Antonioli E, D'Aloia A, Raddino R, Cas LD Tags: Cardiovasc Toxicol Source Type: journals

Severe Impairment of Endothelial Function with the HIV-1 Protease Inhibitor Indinavir is not Mediated by Insulin Resistance in Healthy Subjects.Email this article to a colleague. Save this article to My Clippings. Discuss or comment on this article.
Endothelial dysfunction may contribute to increased cardiovascular events among HIV-1-infected patients receiving antiretroviral therapy. The HIV-1 protease inhibitor indinavir causes both vascular dysfunction and insulin resistance, but the relationship between the two disturbances is not established. Endothelium-dependent vasodilation (EDV), insulin-mediated vasodilation (IMV), and whole body and leg glucose uptake during a euglycemic hyperinsulinemic clamp (40 mU/m(2)/min) were measured before and after four weeks of indinavir in nine healthy men. EDV fell from 270 +/- 67% above basal to 124 +/- 30% (P = 0.04) and I...
Source: Cardiovascular Toxicology - July 16, 2008 Category: Cardiology Authors: Dubé MP, Gorski JC, Shen C Tags: Cardiovasc Toxicol Source Type: journals

Adhesion proteins, stem cells, and arrhythmogenesis.Email this article to a colleague. Save this article to My Clippings. Discuss or comment on this article.
Cell-transplantation therapy is a promising treatment option that is being actively explored as a way to repair cardiac muscle. The ultimate goal is to reconstitute the architecture of the cardiac muscle and to reestablish electrical propagation, while avoiding hypertrophy and scar formation. In this review, we focus on recent advances in the field as well as the difficulties encountered when the engraftment of cells into the host tissue is to be confirmed and functionally characterized. This is critical since incomplete or partial engraftment of transplanted cells within the host cardiac network exacerbates the hetero...
Source: Cardiovascular Toxicology - July 16, 2008 Category: Cardiology Authors: Gillum N, Sarvazyan N Tags: Cardiovasc Toxicol Source Type: journals

An Unusual CO-conspirator in a Case of Acute Coronary Syndrome.Email this article to a colleague. Save this article to My Clippings. Discuss or comment on this article.
We present the case of a young man with CO poisoning who had elevated cardiac biomarkers, a regional wall motion abnormality, and was found to have obstructive coronary disease. Evidence of myocardial necrosis in the setting of CO toxicity should prompt consideration of an evaluation for coronary artery disease, particularly among those with risk factors. PMID: 18273709 [PubMed - in process] (Source: Cardiovascular Toxicology)
Source: Cardiovascular Toxicology - July 16, 2008 Category: Cardiology Authors: Monahan K, Eshaghian A, Dixon J Tags: Cardiovasc Toxicol Source Type: journals

Differential Phosphorylation of Translation Initiation Regulators 4EBP1, S6k1, and Erk 1/2 Following Inhibition of Alcohol Metabolism in Mouse Heart.Email this article to a colleague. Save this article to My Clippings. Discuss or comment on this article.
Acute alcohol intoxication leads to an inhibition of protein synthesis in heart that results in part through altered phosphorylation of protein factors controlling mRNA translation initiation. The purpose of the present set of experiments was designed to examine the effects of inhibitors of ethanol metabolism on the phosphorylation of 4E-binding protein (4EBP1) and S6k1(Thr(389)), two factors regulating mRNA translation initiation. Phosphorylation of 4E-BP1, S6k1(Thr(389)), and Erk 1/2 was reduced 2 h following IP injection of alcohol. Pretreatment with 4-methylpyrazole (4-MP), an inhibitor of alcohol dehydrogenase (AD...
Source: Cardiovascular Toxicology - July 16, 2008 Category: Cardiology Authors: Vary TC, Lang CH Tags: Cardiovasc Toxicol Source Type: journals

Trichloroethylene and trichloroacetic Acid regulate calcium signaling pathways in murine embryonal carcinoma cells p19.Email this article to a colleague. Save this article to My Clippings. Discuss or comment on this article.
In this study, we investigated the global changes in gene expression caused by exposure of P19 embryonal carcinoma cells to TCE and TCA, and whether or not TCE and/or TCA influence the expression levels of genes encoding for proteins that regulate calcium fluxes in cardiac cells. We report that TCE and TCA disrupt the expression of genes involved in processes important during embryonic development suggesting that exposure to environmentally significant concentrations of TCE may have deleterious effects on specific stages of cardiac differentiation. PMID: 18437584 [PubMed - in process] (Source: Cardiovascular Toxicology)
Source: Cardiovascular Toxicology - July 16, 2008 Category: Cardiology Authors: Selmin OI, Thorne PA, Caldwell PT, Taylor MR Tags: Cardiovasc Toxicol Source Type: journals

Cardiac-Targeted Transgenic Mutant Mitochondrial Enzymes: mtDNA Defects, Antiretroviral Toxicity and Cardiomyopathy.Email this article to a colleague. Save this article to My Clippings. Discuss or comment on this article.
Mitochondrial (mt) DNA biogenesis is critical to cardiac contractility. DNA polymerase gamma (Pol gamma) replicates mtDNA, whereas thymidine kinase 2 (TK2) monophosphorylates pyrimidines intramitochondrially. Point mutations in POLG and TK2 result in clinical diseases associated with mtDNA depletion and organ dysfunction. Pyrimidine analogs (NRTIs) inhibit Pol gamma and mtDNA replication. Cardiac "dominant negative" murine transgenes (TGs; Pol gamma Y955C, and TK2 H121N or I212N) defined the role of each in the heart. mtDNA abundance, histopathological features, histochemistry, mitochondrial protein abundance, morphome...
Source: Cardiovascular Toxicology - July 16, 2008 Category: Cardiology Authors: Kohler JJ, Hosseini SH, Green E, Hoying-Brandt A, Cucoranu I, Haase CP, Russ R, Srivastava J, Ivey K, Ludaway T, Kapoor V, Abuin A, Shapoval A, Santoianni R, Saada A, Elpeleg O, Lewis W Tags: Cardiovasc Toxicol Source Type: journals

Nuclear factor e2-related factor 2-dependent myocardiac cytoprotection against oxidative and electrophilic stress.Email this article to a colleague. Save this article to My Clippings. Discuss or comment on this article.
This study was undertaken to investigate if Nrf2 signaling could control the constitutive and inducible expression of antioxidants and phase 2 enzymes in primary cardiomyocytes as well as the susceptibility of these cells to oxidative and electrophilic injury. The basal expression of a series of antioxidants and phase 2 enzymes was significantly lower in cardiomyocytes from Nrf2(-/-) mice than those from wild-type littermates. Incubation of wild-type cardiomyocytes with 3H-1,2-dithiole-3-thione (D3T) led to significant induction of various antioxidants and phase 2 enzymes, including catalase, glutathione, glutathione perox...
Source: Cardiovascular Toxicology - July 16, 2008 Category: Cardiology Authors: Zhu H, Jia Z, Misra BR, Zhang L, Cao Z, Yamamoto M, Trush MA, Misra HP, Li Y Tags: Cardiovasc Toxicol Source Type: journals

Analysis of prevalence and risk factors of hypertension among uygur adults in tushala and hetian xinjiang uygur autonomous region.Email this article to a colleague. Save this article to My Clippings. Discuss or comment on this article.
In conclusion, our results indicated that high caloric food intake may trigger hyperlipidemia and subsequently elevated blood pressure, with elevated BMI and cholesterol levels being the major risk factors for hypertension. PMID: 18483876 [PubMed - in process] (Source: Cardiovascular Toxicology)
Source: Cardiovascular Toxicology - July 16, 2008 Category: Cardiology Authors: Li LL, Liu XY, Ran JX, Wang Y, Luo X, Wang T, Ren J, Aisha M, Abudureheman R, Xiawudong A, Zhang XC, Mao XM Tags: Cardiovasc Toxicol Source Type: journals

Inhibitors of GSK-3 Prevent Corticosterone from Inducing COX-1 Expression in Cardiomyocytes.Email this article to a colleague. Save this article to My Clippings. Discuss or comment on this article.
Our recent study has demonstrated that glucocorticoids (GCs) induce cyclooxygenase-1 (COX-1) gene expression in rat cardiomyocytes. While investigating the mechanism underlying corticosterone (CT) induced COX-1, we found that three structurally and mechanistically distinct GSK-3 inhibitors, LiCl, SB216763, and (2'Z,3'E)-6-Bromoindirubin-3'-oxime (BIO), inhibited COX-1 transcription and protein induction. A genetic approach of expressing wild type GSK-3beta increased COX-1 promoter activity, which was abolished by LiCl. LiCl increased inhibitory GSK-3alpha/beta phosphorylation at Ser21/Ser9, while BIO or SB216763 preven...
Source: Cardiovascular Toxicology - July 16, 2008 Category: Cardiology Authors: Sun H, Chen QM Tags: Cardiovasc Toxicol Source Type: journals

Potent Induction of Total Cellular and Mitochondrial Antioxidants and Phase 2 Enzymes by Cruciferous Sulforaphane in Rat Aortic Smooth Muscle Cells: Cytoprotection Against Oxidative and Electrophilic Stress.Email this article to a colleague. Save this article to My Clippings. Discuss or comment on this article.
Sulforaphane, a cruciferous isothiocyanate compound, upregulates cytoprotective genes in liver, but its effects on antioxidants and phase 2 defenses in vascular cells are unknown. Here we report that incubation of rat aortic smooth muscle A10 cells with sulforaphane (0.25-5 muM) resulted in concentration-dependent induction of a spectrum of important cellular antioxidants and phase 2 enzymes, including superoxide dismutase (SOD), catalase, the reduced form of glutathione (GSH), glutathione peroxidase, glutathione reductase (GR), glutathione S-transferase (GST), and NAD(P)H:quinone oxidoreductase 1 (NQO1). Sulforaphane ...
Source: Cardiovascular Toxicology - July 8, 2008 Category: Cardiology Authors: Zhu H, Jia Z, Strobl JS, Ehrich M, Misra HP, Li Y Tags: Cardiovasc Toxicol Source Type: journals

Chronic Contamination of Rats with (137)Cesium Radionuclide: Impact on the Cardiovascular System.Email this article to a colleague. Save this article to My Clippings. Discuss or comment on this article.
Cardiovascular system impairment has been observed in children and in liquidators exposed to the Chernobyl nuclear power plant accident. No experimental studies of animals have analyzed whether these disorders might be attributed to chronic ingestion of low levels of cesium 137 ((137)Cs). Biochemical, physiological, and molecular markers of the cardiovascular system were analyzed in rats exposed through drinking water to (137)Cs at a dose of 500 Bq kg(-1) (6500 Bq l(-1)). Plasma concentrations of CK and CK-MB were higher (+52%, P < 0.05) in contaminated rats. No histological alteration of the heart was observed, but...
Source: Cardiovascular Toxicology - March 1, 2008 Category: Cardiology Authors: Guéguen Y, Lestaevel P, Grandcolas L, Baudelin C, Grison S, Jourdain JR, Gourmelon P, Souidi M Tags: Cardiovasc Toxicol Source Type: journals

Reduction of protein synthesis and statin-induced cardiomyocyte cell death.Email this article to a colleague. Save this article to My Clippings. Discuss or comment on this article.
The objective of this study was to determine whether an HMG Co A reductase inhibitor (statin) reduces protein synthesis in cardiomyocytes and whether this action maybe an underlying mechanism for statin-induced cell death. Cardiomyocytes from embryonic chick heart were maintained in culture. Cells exposed to lovastatin for 4 h showed a concentration dependent reduction in protein synthesis as assessed by [3H] leucine incorporation and [35S] methionine incorporation. Compared to control, lovastatin 100 microM, which produced a 25% increase in cell death, induced a three-fold reduction in methionine incorporation. [35S] meth...
Source: Cardiovascular Toxicology - January 1, 2007 Category: Cardiology Authors: Rabkin SW, Lodha P, Kong JY Tags: Cardiovasc Toxicol Source Type: journals

Impact of Pycnogenol on cardiac extracellular matrix remodeling induced by L-NAME administration to old mice.Email this article to a colleague. Save this article to My Clippings. Discuss or comment on this article.
Cardiac remodeling is a determinant of the clinical progression of heart failure and now slowing or reversing remodeling is considered as a potential therapeutic target in heart failure. Pycnogenol has been reported to mediate a number of beneficial effects in the cardiovascular system but its effects on hemodynamic and functional cardiovascular changes following cardiac remodeling have not been elucidated. Therefore, we investigated the influence of Pycnogenol supplementation (30 mg/kg) on left ventricular function and myocardial extracellular matrix composition in old C57BL/6N mice following induction of cardiac remo...
Source: Cardiovascular Toxicology - January 1, 2007 Category: Cardiology Authors: Zibadi S, Yu Q, Rohdewald PJ, Larson DF, Watson RR Tags: Cardiovasc Toxicol Source Type: journals