Effect of Captopril on Nitric Oxide and Its Synthase Activity During Myocardial Ischemia-reperfusion in Rat Heart

ObjectiveTo study the effect of myocardial nitric oxide (NO) and nitric oxide synthase (NOS) in myocardial ischemia-reperfusion injury and evaluate the mechanism of cardioprotection of captopril on myocardial ischemia-reperfusion injury in rat heart. MethodsThe isolated Langendorff perfused rat heart model was used. Rat hearts were randomly divided into three groups (6 in each group): control group, ischemia-reperfusion (I/R) group and captopril group. NOS isoenzyme activity, superoxide dismutase(SOD) activity, malondialdehyde(MDA) content, creatine phosphokinase(CK)content and the changes of NO content in coronary effluent during reperfusion were observed.ResultsMyocardial inducible NOS (iNOS) activity in I/R group was increased than that of control group, however myocardial constitutive NOS(cNOS) activity and total NOS activity decreased significantly (P0.001,0.05)after myocardial reperfusion and NO content in coronary effluent reduced (P0.01) in I/R group. Captopril group presented lower myocardial iNOS activity (P0.01) and higher cNOS and total NOS activity (P0.01,0.05) 30 min after reperfusion. NO content in coronary effluent in captopril group maintained higher level (P0.01) during reperfusion, these were compared with I/R group .And myocardial injury in captopril group was ameliorated. ConclusionsThe abnormality of myocardial NOS isoenzyme activity and NO production may be one of the important factors inducing myocardial I/R injury.The myocardial protection mechanism of captopril may be attributed to its effect on maintaining normal NO level by regulating myocardial NOS isoenzyme activity.