INCREASED VULNERABILITY OF HYPERTROPHIED MYOCARDIUM TO ISCHEMIA AND REPERFUSION INJURY - RELATION TO CARDIAC RENIN-ANGIOTENSIN SYSTEM

Hearts of pressure-overload hypertrophy show an increased activation o f intracardiac renin-angiotensin system which may contribute to ischem ia and reperfusion injury. The purpose of this study is to evaluate wh ether the hypertrophied myocardium is more vulnerable to ischemia and reperfusion injury and to find out its relation to the cardiac renin-a ngiotensin system. Hypertrophied rat hearts induced by abdominal aorti c banding for 6 weeks were subjected to 2 hours of hypothermic ischemi c arrest followed by 30 minutes of reperfusion, and their cardiac func tion recovery was compared with that of sham-operated normal control h earts. The cardiac renin activity and angiotensin II content before is chemia and after reperfusion were determined. It was found that both t he pre-ischemic renin activity and angiotensin II level were higher in hypertrophied myocardium than those in the control: ischemia and repe rfusion injury increased both renin activity and angiotensin II conten t in the two groups, but the renin activity and angiotensin II level w ere further elevated after reperfusion in the hypertrophied hearts tha n those in the control hearts. Meanwhile, the cardiac function recover y after 30 minutes reperfusion in the hypertrophied hearts was poorer than that in the control. Correlation analysis revealed that there was a negative correlation between the cardiac output recovery and the my ocardial angiotensin II content (r=-0.841), P<0.001), It is concluded that ischemia and reperfusion injury can activate cardiac renin-angiot ensin system in isolated rat heart, which may be responsible for the i ncreased susceptibility of the hypertrophied myocardium to ischemia an d reperfusion injury.