Study On Ischemia-Reperfusion Injury In The Hypertrophied Myocardium

The hypertrophied myocardium increases the vulnerability to ischemia-reperfusion injury and may consequently be associated with: (1). the increasing mortality, myocardial infarct size and incidence of sudden death; (2). the increase of the cardiac operative mortality and the prevalence of postoperative complications. Recently, some evidences suggest that the cardiac renin-angiotensin system(RAS) may be involved in the myocardial ischemia-reperfusion injury as well as in the cardiac hypertrophy. The increase of intracardiac activation of RAS in hypertrophied myocardium would in turn contribute to the increasing susceptibility to ischemia-reperfusion injury. In order to verify the above hypothesis and to determine whether the specific inhibition of the cardiac RAS by captopril would modify ischemia-reperfusion injury of the hypertrophied myocardium, the investigations in the isolated pressure overload hypertrophied rat hearts were as follows:1. Cardiac RAS and myocardial hypertrophy: The pressure overload myocardial hypertrophy was induced in rats by abdominal aortic banding for 6 weeks. Compared with the sham-operated control hearts, the renin activity and the All content increased in the hypertrophied hearts, but no difference was found in the plasma All level. Correlation analysis revealed that the myocardial All was positively related to the cardiac mass, suggesting that the cardiac RAS may be involved in the myocardial hypertrophy. Results also showed that the Na and Ca in the hypertrophied myocardium increased while K content decreased. The imbalance of these electrolytes may be the electrophysiological basis for inducing arrythmia.2. Ischemia-reperfusion injury of the hypertrophied myocardium: Isolated rat hearts were subjected to 2hrs cardioplegic arrest at 22'C and then followed by 30 min of reperfusion. Compared with the control hearts, the hypertrophied hearts presented deteriolated cardiac function recovery and were associated with greater increase of coronary resistance, myocardial lactate, and Na, Ca and water content. The CF was markedly depressed and the peak CPK release was postponed. The results confirmed that the hypertrophied hearts were more vulnerable to ischemia-reperfusion injury in this experimental condition.