Effects of captopril on enzymatology of cultured anoxic-reperfused ventricular myocardial cells

AIM To investigate the effects of captopril on the enzymatology of cultured anoxicreperfused ventricular myocardial cells. METHODS An anoxicreperfusion model was established by using cultured ventrical myocardial cells of neonate rats. The CPK, ALP, AST, LDH and ACE activity in medium of myocardial cells was measured for 60, 120 and 180 min after anoxia and 30 and 60 min after reperfusion and the effects of 0.5 mg·L -1 captopril on anoxicreperfused myocardial cells were studied. RESULTS The release of CPK, ALP, AST, LDH and ACE from the myocardial cells increased gradually as anoxia and reperfussion prolonged. In the early period of anoxia, the level of CPK and ALP was a more sensitive indicator of the extent of injury to the myocardial cells than that of AST and ACE. Meanwhile, 0.5 mg·L -1 captopril might reduce the leakage of enzymes significantly during anoxia and reperfussion. CONCLUSION That captopril might reduce the leakage of enzymes of cultured myocardial cells demonstrated that captopril might have a direct protective effect on myocardial cells afflicted with anoxicreperfusion injury.