Effects of perindopril on left ventricular remodeling and myocardial osteopontin expression in rats with myocardial infarction / 南方医科大学学报

ABSTRACT

<p><b>OBJECTIVE</b>To observe the effects of perindopril on left ventricular remodeling and myocardial osteopontin expression in rats with myocardial infarction (MI).</p><p><b>METHODS</b>Male adult SD rats were randomly divided into sham-operation group, MI-saline group and MI-perindopril group, and in the latter two groups, ligation of the left anterior descending artery was performed to establish rat models of myocardial infarction and perindopril (2 mg/kg daily) or saline was administered since the next day of MI. Four weeks later, the left ventricular diameter (LVEDD and LVESD) and left ventricular ejection fraction were estimated with echocardiography, and the left ventricular systolic pressure (LVSP), left ventricular end-diastolic pressure (LVEDP) and -/+dp/dt(max) was obtained via hemodynamic measurement, with also evaluation of the cardiac myocyte diameter and interstitial fibrosis infiltration with histological methods. Western blotting was performed to detect the expression level of myocardium osteopontin protein.</p><p><b>RESULTS</b>Compared with the sham-operation group, all MI rats developed significant systolic and diastolic dysfunction, as indicated by decreased LVEF, LVSP and -/+dp/dt(max), as well as increased LVEDP. MI rats showed significantly dilated left ventricles and higher ventricular weight/body weight ratio, significantly increased cardiomyocyte diameter and marked interstitial fibrosis in the non-infarction area. Perindopril treatment partially prevented cardiac dysfunction and left ventricular remodeling as indicated by the above indices. No osteopontin was detected in the myocardium of sham-operation rats, and in MI rats, high level of osteopontin expression, as detected in MI-saline group, was significantly inhibited by perindopril treatment.</p><p><b>CONCLUSION</b>Perindopril treatment can significantly inhibit left ventricular remodeling and myocardium osteopontin expression in rats with MI.</p>