目的：探讨卡托普利（ｃａｐｔｏｐｒｉｌ）对局部缺血再灌注免心肌保护作用的机制。 方法：将１８只新西兰兔随机分３组（每组ｎ＝６），对照组左冠状动脉前降支阻断３０分，再灌注９０分；卡托普利组阻断前３０分静脉注射卡托普利每 ２０分 ２ ｍｇ／ｋｇ，再灌注时再持续静脉注射卡托普利每 ９０分１ｍｇ／ｋｇ，假手术组环左冠状动脉前降支置线但不阻断血流。观察心肌一氧化氮合酶（ＮＯＳ）同工酶活性、过氧化物歧化酶活性、丙二醛含量、肌酸激酶含量及右心房血一氧化氮（ＮＯ）的变化，监测心肌功能。 结果：缺血再灌注心肌原生型ＮＯＳ（ＣＮＯＳ）活性（Ｐ＜０．００１）及总ＮＯＳ活性（Ｐ＜０．０１）显著下降，ＮＯ产生减少（Ｐ＜０．０５～０．０１），卡托普利组缺血再灌注期间ＮＯ水平高于对照组（Ｐ＜０．０１），再灌注３０分心肌ＣＮＯＳ活性（Ｐ＜０．０１）及总ＮＯＳ活性（Ｐ＜０．０５）显著高于对照组，心肌损害较对照组减轻。 结论：ＮＯ产生不足是心肌再灌注损伤的重要因素，卡托普利通过调节ＮＯＳ活性，维持正常ＮＯ水平起到保护作用。 Objective: To investigate the mechanism of captopril on myocardial protection against ischemia-reperfusion injury. Methods: 18 New Zealand white rabbits were randomly divided into 3 groups (n = 6 in each group). The left anterior descending coronary artery of the control group was blocked for 30 minutes and then reperfused for 90 minutes. In the captopril group, Toplite every 20 minutes 2 mg / kg, reperfusion, continuous intravenous captopril every 90 minutes 1mg / kg, sham group left anterior descending coronary artery ring set line but does not block the blood flow. Myocardial nitric oxide synthase (NOS) isoenzyme activity, superoxide dismutase activity, malondialdehyde content, creatine kinase content and right atrial blood nitric oxide (NO) were measured to observe myocardial function. Results: The activity of NOS (P <0.001) and total NOS (P <0.01) in myocardial ischemic reperfusion group were significantly decreased and NO production was decreased (P <0.05 ~ 0.01) The level of NO in captopril group was significantly higher than that in control group during reperfusion (P <0.01). The activity of CNOS (P <0.01) and total NOS activity (P <0.05) Higher than the control group, myocardial damage than the control group. CONCLUSION: Insufficient NO production is an important factor of myocardial reperfusion injury. Captopril can protect normal NO level through regulating NOS activity.