【摘要】 目的　探讨体外反搏对心肌缺血时犬血管紧张素转换酶 (ACE)的影响及机制。方法　采用冠状动脉结扎法复制犬急性心肌缺血模型 ,外加反搏治疗 ,观测犬血流动力学指标及缺血心肌、主动脉局部血管紧张素Ⅱ水平、ACE活性的改变 ,用RT PCR方法检测局部ACEmRNA的表达。结果体外反搏能改善犬左心室舒缩功能 ,抑制缺血激活的缺血心肌、主动脉处ACE活性及血管紧张素Ⅱ水平 ,抑制缺血心肌、主动脉处ACEmRNA的表达。结论　体外反搏能通过抑制心血管局部ACE的表达抑制局部肾素 血管紧张素系统 ,这可能是体外反搏保护缺血心肌的作用机制之一更多还原

【Abstract】 Objective To probe the effects of external counterpulsation (ECP) on angiotensin-converting enzyme (ACE) in dogs with myocardial ischemia(MI) and its mechanism. Methods Eighteen dogs were divided into sham, MI, MI+ECP groups. Acute myocardial ischemia was induced by occluding the left anterior descending coronary artery. The ischemic and ECP group was treated by ECP after 1h MI. The local renin activity, angiotensin II (Ang II) level, ACE activity in ischemic myocardium and aorta were tested by biochemical way. The hemodynamics were recorded by a 8-channel physiological recorder. The expression of local ACE mRNA was tested by RT-PCR. Results ECP could improve the function of contraction and diastole of the left ventricle, reduce cardiovascular ANG II level and ACE activity, which were activated by ischemia, reduce the expression of local ACE mRNA in ischemic myocardium and aorta [(myocardium: (0.90±0.08) vs (0.77±0.10), aorta: (1.42±0.27) vs (1.20±0.14)]. The local ACE activity was closely related to the local ACE mRNA (r=0.903). Conclusion ECP can depress the local RAS by depressing their gene expression, which may be one of the mechanisms of ECP protection for ischemic myocardium.更多还原