对体外反搏提高切应力抑制血管紧张素转换酶的探讨

目的　通过观察体外反搏对心肌缺血犬血管切应力和局部血管紧张素转换酶的影响 ,探讨其保护缺血心肌的机制。方法　采用冠状动脉结扎法复制犬急性心肌缺血模型 ,外加体外反搏治疗 ,观测缺血及反搏过程中头背干动脉切应力与缺血心肌、主动脉局部ANGⅡ水平、ACE活性的改变 ,分析主动脉ACE活性与头背干动脉切应力之间的关系。结果　反搏能提高缺血降低的切应力使之达正常水平 ;还能抑制缺血激活的缺血心肌与主动脉ACE活性、ANGⅡ水平 ,其中主动脉ACE活性达正常水平 ;主动脉ACE活性与头背干动脉切应力有相关关系。结论　体外反搏能抑制心血管局部肾素 血管紧张素系统 ,提高切应力 ,且二者有相关关系 ,这可能是体外反搏保护缺血心肌的作用机制之一

Study on suppression of angiotensin-converting enzyme by increased shear stress induced by external counterpulsation

Objective To probe the mechanism of protective effect of external counterpulsation(ECP) on ischemic myocardium by observing its effect on local angiotensin converting enzyme(ACE) and vascular shear stress in dogs with myocardial ischemia(MI).Methods Eighteen dogs were divided into sham operated,MI and MI+ECP groups. Acute myocardial ischemia was induced by occluding the left anterior descending coronary artery in MI and MI+ECP groups.The MI+ECP group was also treated with ECP after 1h of MI. The local angiotensin(ANGⅡ) level,ACE activity in ischemic myocardium and aorta were measured by biochemical method and blood flow was recorded using a 8 channel physiological recorder.Shear stress was calculated from blood flow.Results ECP could improve shear stress,which decreased significantly with ischemia,to the level of sham operated group. It also could reduce cardiovascular ANGⅡ level and ACE activity which were activated by ischemia. ACE activity in aorta was closely related to shear stress.Conlusions ECP can depress the local renin angiotensin system and increase local shear stress. ACE activity is closely related to shear stress,which may be a mechanism of protection of ischemic myocardium by ECP.