Zhang Y, Xu S
Cardiovascular Institute & Fuwai Hospital, Chinese Academy of Medical Sciences, Beijing.
Chin Med J (Engl). 1995 Jan;108(1):28-32.
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 = -0.8411, 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.
压力超负荷肥大心脏显示心内肾素-血管紧张素系统激活增加，这可能导致缺血和再灌注损伤。本研究的目的是评估肥厚心肌是否更易受缺血和再灌注损伤影响，并找出其与心脏肾素-血管紧张素系统的关系。对通过腹主动脉结扎诱导6周的肥厚大鼠心脏进行2小时低温缺血停搏，随后进行30分钟再灌注，并将其心脏功能恢复情况与假手术正常对照心脏进行比较。测定缺血前和再灌注后心脏肾素活性和血管紧张素II含量。结果发现，肥厚心肌缺血前的肾素活性和血管紧张素II水平均高于对照组：缺血和再灌注损伤使两组的肾素活性和血管紧张素II含量均增加，但肥厚心脏再灌注后的肾素活性和血管紧张素II水平比对照心脏进一步升高。同时，肥厚心脏再灌注30分钟后的心脏功能恢复比对照组差。相关性分析显示心输出量恢复与心肌血管紧张素II含量之间呈负相关（r = -0.8411，P < 0.001）。结论是，缺血和再灌注损伤可激活离体大鼠心脏的心脏肾素-血管紧张素系统，这可能是肥厚心肌对缺血和再灌注损伤易感性增加的原因。
