Myocardial effects of beta-agonist stimulation in rats with chronic left ventricular dysfunction treated with an angiotensin-converting enzyme inhibitor.
{"title":"Myocardial effects of beta-agonist stimulation in rats with chronic left ventricular dysfunction treated with an angiotensin-converting enzyme inhibitor.","authors":"W J Cherng, C H Wang, S F Chen, M J Hung","doi":"","DOIUrl":null,"url":null,"abstract":"<p><strong>Background: </strong>This study measured morphological and hemodynamic changes and renin-angiotensin responsiveness of the left ventricle (LV) to beta-agonist stimulation in a Sprague-Dawley rat model of myocardial dysfunction produced by coronary artery ligation.</p><p><strong>Methods: </strong>The LV function and papillary muscle mechanics were measured after 12 weeks of captopril treatment (2 g/l in drinking water) following left coronary artery ligation or a sham operation. Fifty-two rats were divided into three groups: those with sham operations, those with small infarcts (infarct size [IS] < 30% LV) and those with large infarcts (IS > or = 30% LV).</p><p><strong>Results: </strong>The results showed that LV end-diastolic pressures were elevated in the large-infarct group regardless of treatment with the angiotensin-converting enzyme inhibitor (ACEI), and the LV weight was reduced in the ACEI-treated rats. In addition, the uninfarcted LV posterior papillary muscle of the large-infarct rats showed an impaired response to isoproterenol stimulation, including the developed tension, positive and negative rate of tension development, time to peak tension, and time to half relaxation.</p><p><strong>Conclusion: </strong>Chronic captopril treatment improved isoproterenol-stimulated muscle isometric function in rats following myocardial infarction, possibly through the beta-receptor pathway.</p>","PeriodicalId":77066,"journal":{"name":"Changgeng yi xue za zhi","volume":"22 4","pages":"546-55"},"PeriodicalIF":0.0000,"publicationDate":"1999-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Changgeng yi xue za zhi","FirstCategoryId":"1085","ListUrlMain":"","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
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Abstract
Background: This study measured morphological and hemodynamic changes and renin-angiotensin responsiveness of the left ventricle (LV) to beta-agonist stimulation in a Sprague-Dawley rat model of myocardial dysfunction produced by coronary artery ligation.
Methods: The LV function and papillary muscle mechanics were measured after 12 weeks of captopril treatment (2 g/l in drinking water) following left coronary artery ligation or a sham operation. Fifty-two rats were divided into three groups: those with sham operations, those with small infarcts (infarct size [IS] < 30% LV) and those with large infarcts (IS > or = 30% LV).
Results: The results showed that LV end-diastolic pressures were elevated in the large-infarct group regardless of treatment with the angiotensin-converting enzyme inhibitor (ACEI), and the LV weight was reduced in the ACEI-treated rats. In addition, the uninfarcted LV posterior papillary muscle of the large-infarct rats showed an impaired response to isoproterenol stimulation, including the developed tension, positive and negative rate of tension development, time to peak tension, and time to half relaxation.
Conclusion: Chronic captopril treatment improved isoproterenol-stimulated muscle isometric function in rats following myocardial infarction, possibly through the beta-receptor pathway.