摘要
目的 :探讨心肌缺血与体外反搏 (ECP)时犬心肌肾素 -血管紧张素系统 (RAS)、心功能和超微结构的改变以及它们之间的关系。方法 :采用成年杂种犬 17只 ,冠状动脉结扎法复制犬急性心肌缺血模型 ,检测缺血及外加反搏时缺血心肌局部肾素活性、血管紧张素Ⅱ (ANGⅡ )水平和血管紧张素转换酶 (ACE)活性 ,用八导生理记录仪记录±dp/dtmax ,分析它们和ANGⅡ水平之间的关系 ,透射电镜观察心肌超微结构。结果 :缺血能激活缺血或心肌肾素、ACE和ANGⅡ ,反搏对其有一定抑制作用 ;体外反搏能减轻缺血区超微结构的损伤 ;缺血与反搏时心肌舒缩功能的改变和心肌局部ANGⅡ水平有关。结论 :体外反搏治疗心肌缺血时 ,其对心功能的改善作用可能与抑制局部RAS有关 ,这可能是它对缺血心肌起保护作用的机制之一。
Objective:To investigate the effects of external counterpulsation(ECP) on renin angiotensin system(PAS) and heart function in dogs with myocardial ischemia and their relationship.Methods:Acute myocardial ischemia in dogs was induced by occluding the coronary artery.The local renin activity,angiotensin (ANGⅡ) level,ACE activity in ischemic myocardium were determined and ±dp/dt max was recorded using an 8 channel physiological recorder.Myocardial ultrastructure was examined under a transmission electron microscope.Results:Ischemia could activate renin,ACE and ANGⅡ in ischemic myocardium and ECP reduced them.ECP could reduce the injury of the myocardial ultrastructure.ECP also improved ±dp/dt max and there was a close relationship between ±dp/dt max and local ANGⅡ level.Conclusions:The improving effects of ECP on heart function of dogs with myocardial ischemia are correlated with local RAS level.This may be one of the protecting mechanism of ECP in ischemic myocardium.
出处
《广州医学院学报》
2001年第3期23-26,共4页
Academic Journal of Guangzhou Medical College