PROTECTIVE EFFECT OF CAPTOPRIL ON ISCHEMIC MYOCARDIUM

The protective effect and mechanism of action of the angiotensin-conve rting enzyme inhibitor (ACE-I) captopril was investigated in organelle s from ischemic myocardial cells in a canine coronary ligation model. Sarcoplasmic reticulum (SR) and mitochondrial fractions were extracted from ischemic and nonischemic myocardial cells from captopril- and sa line-treated (control) hearts. Heart rate, cardiac output, and right v entricular systolic blood pressure were similar in the captopril-treat ed and control groups. Left ventricular systolic blood pressure (LVPs) decreased gradually to 89% of the baseline value after captopril admi nistration, and to 78% of the baseline value after ligation. Ca-ATPase activity in the SR, the respiratory control ratio (RCR) in the mitoch ondria, and dinitrophenol (DNP)-stimulated ATPase activity were signif icantly higher in ischemic myocardium from the captopril-treated group than from the saline-tseated (control) group. The SH group content of both organelles was higher in the captopril-treated group. Our result s suggest that, in addition to their hemodynamic effects, ACE-I agents containing SH groups protect the myocardium from ischemic damage by p reventing enzyme oxidation.