Hearts of pressure-overload hypertrophy show an increased activation of intracardiac renin-angiotensin system which may contribute to ischemia and reperfusion injury. The purpose of this study is to evaluate whether t...Hearts of pressure-overload hypertrophy show an increased activation of intracardiac renin-angiotensin system which may contribute to ischemia and reperfusion injury. The purpose of this study is to evaluate whether the hypertrophied myocardium is more vulnerable to ischemia and reperfusion injury and to find out its relation to the cardiac renin-angiotensin system. Hypertrophied rat hearts induced by abdominal aortic banding for 6 weeks were subjected to 2 hours of hypothermic ischemic arrest followed by 30 minutes of reperfusion, and their cardiac function recovery was compared with that of sham-operated normal control hearts. The cardiac renin activity and angiotensin II content before ischemia and after reperfusion were determined. It was found that both the pre-ischemic renin activity and angiotensin II level were higher in hypertrophied myocardium than those in the control: ischemia and reperfusion injury increased both renin activity and angiotensin II content in the two groups, but the renin activity and angiotensin II level were further elevated after reperfusion in the hypertrophied hearts than those in the control hearts. Meanwhile, the cardiac function recovery 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 myocardial angiotensin II content (r=-0.841), P<0.001), It is concluded that ischemia and reperfusion injury can activate cardiac renin-angiotensin system in isolated rat heart, which may be responsible for the increased susceptibility of the hypertrophied myocardium to ischemia and reperfusion injury.展开更多
文摘Hearts of pressure-overload hypertrophy show an increased activation of intracardiac renin-angiotensin system which may contribute to ischemia and reperfusion injury. The purpose of this study is to evaluate whether the hypertrophied myocardium is more vulnerable to ischemia and reperfusion injury and to find out its relation to the cardiac renin-angiotensin system. Hypertrophied rat hearts induced by abdominal aortic banding for 6 weeks were subjected to 2 hours of hypothermic ischemic arrest followed by 30 minutes of reperfusion, and their cardiac function recovery was compared with that of sham-operated normal control hearts. The cardiac renin activity and angiotensin II content before ischemia and after reperfusion were determined. It was found that both the pre-ischemic renin activity and angiotensin II level were higher in hypertrophied myocardium than those in the control: ischemia and reperfusion injury increased both renin activity and angiotensin II content in the two groups, but the renin activity and angiotensin II level were further elevated after reperfusion in the hypertrophied hearts than those in the control hearts. Meanwhile, the cardiac function recovery 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 myocardial angiotensin II content (r=-0.841), P<0.001), It is concluded that ischemia and reperfusion injury can activate cardiac renin-angiotensin system in isolated rat heart, which may be responsible for the increased susceptibility of the hypertrophied myocardium to ischemia and reperfusion injury.
