Myocardial Protective Effect Of Captopril On The Ischemia And Reperfusion Injury In The Canine Heart In Vivo

Recently, some evidences suggest that the cardiac renin -angiotensin system (RAS) is activated during the period of ischemia and reperfusion which aggravates the ischemia and reperfusion injury. It has also been demonstrated that angiotensin converting enzyme inhibitor-captopril (Cp1) can inhibit the activation of cardiac RAS, and protect the heart against ischemia and reperfusion injury. In order to verify the myocardial protective effect of captopril on the heart in vivo, the experiments in the canine heart were designed as follows:Part Ⅰ. Selection of reasonable concentration of captopril in cardioplegia and reperfusional bloodThe mean arterial pressure(MAP), myocardial leakage of CK and CK-MB and the change of circulating blood volume in the oxygenator were observed respectively during CPB with different concentrations of captopril (3.1, 3.4, 4.2, 5.3, 7.2 and 10.2 μmol/L) in the cardioplegia and reperfusional blood. The results indicated that captopril 4.2 and 5.3 μmol/L had a less effect on the circulating blood volume and the MAP and had a reasonable decrease of the myocardial leakage of CK and CK-MB. It was suggested that captopril between 4.2 and 5.3 μmol/L would be the reasonable concentrations in the cardioplegia and reperfusional blood for this experimental model.Part Ⅱ .The effects of cardioplegia and reperfusional blood containing 4.6 μ mol/L captopril on the myocardial performances and hemodynamics after cardiac arrestTwenty four mongrel dogs were divided randomly into 3 groups(8 in each group). (Ⅰ) Control, group: Only modified St. Thomas cardioplegia was used; (Ⅱ) Cp1 group: Cp1 was added into the modified St. Thomas cardioplegia the...