Reduction of Myocardial Infarct Size in Rabbits by Ramiprilat

Hartman, J. Craig; Wall, Theron M.; Hullinger, Thomas G.; Shebuski, Ronald J.

doi:10.1097/00005344-199306000-00022

Cited by 134 publications

(78 citation statements)

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“…For example, studies in patients document that the ST segment shift correlates with both metabolic and contractile parameters of myocardial ischemia (32,48,61,62). Therefore, ST segment changes are widely used as an index of myocardial injury resulting from ischemia in experimental animals (52, 57-59, 64, 86).…”

Section: Discussionmentioning

confidence: 99%

Reduced susceptibility to ventricular tachyarrhythmias in rats selectively bred for high aerobic capacity

Lujan

Britton²,

Koch

et al. 2006

American Journal of Physiology-Heart and Circulatory Physiology

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. Reduced susceptibility to ventricular tachyarrhythmias in rats selectively bred for high aerobic capacity. Am J Physiol Heart Circ Physiol 291: H2933-H2941, 2006. First published August 4, 2006 doi:10.1152/ajpheart.00514.2006.-Reperfusion after a brief period of cardiac ischemia can lead to potentially lethal arrhythmias. Human epidemiological studies and experimental work with animals indicate that regular physical activity is associated with reductions in cardiovascular disease (CVD) risk factors and sudden cardiac death. Similarly, artificial selection of rats for high aerobic treadmill-running capacity (high-capacity runners; HCR) has been shown to reduce CVD risk factors relative to rats selected as lowcapacity runners (LCR). Therefore, we tested the hypothesis that HCR, relative to LCR rats, would be less susceptible to ischemiareperfusion-mediated ventricular tachyarrhythmias. To test this hypothesis, we measured the susceptibility to ventricular tachyarrhythmias produced by 3 min of occlusion and reperfusion of the left main coronary artery in conscious LCR and HCR rats. Results document a significantly lower incidence of ventricular tachyarrhythmias in HCR (3 of 11, 27.3%) relative to LCR (6 of 7, 85.6%) rats. The decreased susceptibility to tachyarrhythmias in HCR rats was associated with a reduced cardiac metabolic demand during ischemia (lower rate-pressure product and ST segment elevation) as well as a wider range for the autonomic control of heart rate. The HCR and LCR represent a unique substrate for evaluation of the mechanisms underlying ischemia-mediated cardiac arrhythmogenesis. artificial selection; cardiovascular risks; arrhythmia; exercise TEMPORARY OCCLUSION of the coronary arteries can lead to potentially lethal arrhythmias (66,82). Coronary artery occlusion-induced arrhythmias are triggered by the ischemic insult directly or on relief of the ischemic insult during the reperfusion phase. The mechanisms underlying the ventricular arrhythmias during ischemia and reperfusion are related but distinct (5,56,75,82). Although ischemia is a more common trigger of sudden death than is reperfusion, life-threatening reperfusion arrhythmias are observed during relief of coronary spasm, during angioplasty or thrombolysis, and after cardiac surgery with ischemic arrest (24).

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Section: Discussionmentioning

confidence: 99%

Reduced susceptibility to ventricular tachyarrhythmias in rats selectively bred for high aerobic capacity

Lujan

Britton²,

Koch

et al. 2006

American Journal of Physiology-Heart and Circulatory Physiology

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“…Pretreatment of rats with captopril It is well known that ACE activity in the myocardium and Ang-II levels in plasma and cardiac tissues increase after acute myocardial ischemia. [1][2][3][4] Increased ACE activity also leads to increased breakdown of bradykinin. These neuro-hormonal changes may exacerbate myocardial ischemia and cause expansion of the infarcted area.…”

Section: Discussionmentioning

confidence: 99%

“…[1][2][3][4] ACE gene deletion polymorphism, which relates to a high plasma level of ACE, has been reported to be associated with a high risk of myocardial infarction and sudden death. [5][6][7][8] Many studies show that ACE activity and angiotensin-II (Ang-II) levels increase in plasma after acute myocardial ischemia, which may lead to exacerbation of myocardial ischemia, cardiac dysfunction and expansion of infarct size.…”

Section: Introductionmentioning

confidence: 99%

“…4,[9][10][11] A large body of data indicates that ACE inhibitors protect myocardium against ischemia/reperfusion in in vitro and in vivo animal models. [2][3][4][12][13][14] Several clinical trials have ted with evidence of lipid peroxidation and enzyme leakage (MDA and LDH levels in the myocardium) and up-regulation of ACE protein expression. Administration of AS-ODN or captopril, but not IN-ODN, reduced Ang-II levels in the plasma, decreased ischemia/reperfusion-mediated cardiac functional deterioration and lipid peroxidation, and preserved LDH in the myocardium (all P Ͻ 0.05 versus the saline group).…”

Section: Introductionmentioning

confidence: 99%

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Protection against ischemia/reperfusion injury and myocardial dysfunction by antisense-oligodeoxynucleotide directed at angiotensin-converting enzyme mRNA

Chen

Mohuczy

et al. 2001

Gene Ther

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Angiotensin-converting enzyme (ACE) activity in the myocardium and angiotensin-II (Ang-II) levels in plasma increase after myocardial ischemia, which lead to exacerbation of myocardial injury and cardiac dysfunction. We examined the protective role of novel antisense-oligodeoxynucleotide (AS-ODN) directed at ACE mRNA in myocardial ischemic injury. Sprague-Dawley rats were treated with ACE-AS-ODN (200 g per rat, n = 8, i.v.) or inverted-ODN (IN-ODN, 200 g per rat, n = 8, i.v.), given with 600 g per rat of liposome DOTAP/DOPE. Hearts from AS-ODN-or IN-ODNtreated rats were excised, perfused in vitro, and subjected to 25 min of global ischemia followed by 30 min of reperfusion. Parallel groups of rats were given ACE inhibitor captopril (5 mg/kg, n = 8) or saline (n = 8) before excising the hearts. Ischemia/reperfusion resulted in myocardial dysfunction (increase in coronary perfusion pressure and LV end-diastolic pressure and a decrease in developed LV pressure) in the saline-treated rats. Myocardial dysfunction was associa-

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“…These effects involve blocking not only angiotensin II formation but also kinin degradation (101,142,143,145,302,311); moreover, they may conceivably be mediated in part via a kinin-NO-dependent mechanism, since they were suppressed by blocking synthesis of NO or prostaglandins (140,144) and diminished in eNOS gene KO mice (313). In animal models of ischemia/reperfusion injury, ACE inhibitors reduced infarct size and ventricular arrhythmias and these effects were attenuated or abolished by co-administering a B 2 antagonist (163) or deleting the TK gene (95,169).…”

Section: Role Of Kinins In Myocardial Ischemia and The Protective Effmentioning

confidence: 99%

The Kallikrein-Kinin System as a Regulator of Cardiovascular and Renal Function

Carretero¹,

Yang²,

Rhaleb³

2005

Hypertension

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Reduction of Myocardial Infarct Size in Rabbits by Ramiprilat

Cited by 134 publications

References 0 publications

Reduced susceptibility to ventricular tachyarrhythmias in rats selectively bred for high aerobic capacity

Reduced susceptibility to ventricular tachyarrhythmias in rats selectively bred for high aerobic capacity

Protection against ischemia/reperfusion injury and myocardial dysfunction by antisense-oligodeoxynucleotide directed at angiotensin-converting enzyme mRNA

The Kallikrein-Kinin System as a Regulator of Cardiovascular and Renal Function

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