Objective: This study was to evaluate the mechanism of protective effects of captopril on myocardium after regional ischemia-reperfusion(I/R) in rabbits. Methods:Myocardial ischemia was induced by ligation of left anterior descending (LAD) artery for 30min followed by 90 min reperfusion (control group,n=6). Captopril of 2 mg/kg within 20min was infused i. v. 30min before LAD oc- clusion and 1 mg/kg within 90 min was again given continuously during the reperfusion period (captopril group,n=6). Rabbits without LAD occlusion were taken as sham group (sham operation group,n=6). Myocardial nitric oxide (NO) synthase (NOS) isoenzyme activity, superoxide dismutase (SOD) activity, malondialdehyde (MDA) content, creatine phosphokinase (CPK) content and the change of the blood levels of NO in right atrium were observed,and the assess- ment of heart function was performed. Results: Myocardial constitutive NOS (cNOS) titutive activity (p<0. 001 ) and total NOS activity (p<0. 01 )de- creased significantly after I/R. NO production was reduced during I/R (p<0.05-0. 01) in control group NO level dur- ing I/R increased significantly(p<0. 01),and myocardial cNOS (p<0. 01) and total NOS (p<0.05) 30min after reper- fusion maintained higher activities in captopril group. These were compared with control group and myocardial injury was alleviated. Conclusion:The deficiency of NO production maybe one of the important factors inducing myocardial I/R injury. The mycardial protection mechanism of captopril maybe be attributed to its effect on maintaining normal No level by increasing cNOS activity.