Myocardial Protective Effect Of Captopril On The Hypothermic Ischemic And Reperfusion Injury In The Isolated Rabbit Heart

The myocardiai protective effect of captopril and its mechanism were investigated through the studies of cardiac function recoveries, biochemical changes, ultrastructural changes and the amount of MDA , PG(?)2. TXA2, renin , angiotensin and electrolytes in the isolated rabbit heart after hypothermic (13 C) ischemic arrest for 3 hours and then reperfusion (37 C) for 35 minutes. Rabbits were randomly divided into 3 ischemic groups and 3 reperfusion groups (8 in each), In the ischemic control group , the hearts were protected by the modified St(?) Thomas cardioplegic solution No 1 only, while in the captopril ischemic groups, the cardiopiegic solutions contained 2.3 and 23.0 umol/L captopril respectivily. In the reperfusion control groups, the heart were protected by cardiopleg(?)a and reperfused by K-H solution, While in captopr(?) reperfusion groups, the cardioplegic soiution and reperfusing K-(?) soiution contained captopril 2.3 or 23.0 uml/L.The results showed that captopril increased the percentage recoveries of the left ventricular peak systolic pressure, +dp/dtmax, -dp/dtmax, coronary flow in the Langendorff aode perfused rabbit heart. Captopri! also improved the cardiac function in the isolated working ra(?)it heart.This was manifested by increasing of left ventricular peak systoiic pressure, +dp/dt max, -dp/dtmax, coronary flow, aortic flow, cardiac output, stroke volume, stroke volume index and reduction of coronary resistance during reperfusion. Captopri! aiso reduced the release of creatine phosphate kinase, the content of lactate in ischeaic myocardium, the content of tissue water of the myocardium. The mitochondial ultrastructure was aiso much better preserved in captopriml groups than that in control groups.The mechanism of the myocardia(?) protective effect of captopril has been investigated. The results showed that captopril decreased the level(?) of iocal angiotensin li and increased renin activity of the myocardium; increased the level of PGI2 and TXA2 at the same time, especially for the level of PGI2, so increased the ratio of PGI2/TXA2 of the myocardium. Captopril reduced the amount of MDA in reperfusion myocardium, but not ischemic myocardium. Captopril decreased the content of Ca2+ and Na+ in the myocardium. Correlation analysis showed that myocardiai contractive function was correlated with the content of MDA,...