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目的：研究心肌局部肾素、血管紧张素Ⅱ（ＡＮＧ－Ⅱ）及去甲肾上腺素（ＮＥ）在心肌晕厥发病中的作用，以及血管紧张素转换酶抑制剂（ＡＣＥＩ）巯甲丙脯酸对心肌缺血－再灌注损伤是否具有保护作用．方法：采用冠状动脉结扎法建立兔心肌晕厥模型，用放射免疫分析法测定心肌晕厥发生时心肌组织肾素，ＡＮＧ－Ⅱ及ＮＥ的变化，缺血前用巯甲丙脯酸静脉给药．结果：心肌缺血后局部肾素活性有升高趋势，再灌注后心肌局部肾素活性有升高趋势，再灌注后心肌局部肾素活性［（６０９．３±２１０）ｐｇ·ｍｇ－１蛋白·ｈ－１］显著高于正常对照组［（１９６．４±２４．８）ｐｇ·ｍｇ－１蛋白·ｈ－１］（Ｐ＜０．０１）．心肌局部ＡＮＧ－Ⅱ含量［（３００５．１±８３５．３）ｐｇ／ｍｇ蛋白］明显高于正常对照组［（１５３５．４±２５８．３）ｐｇ／ｍｇ蛋白］（Ｐ＜０．０１）．心肌ＮＥ含量［（３．０±１．０）μｇ／ｇ湿重ｖｓ（１．１８±０．２８）μｇ／ｇ湿重］明显升高（Ｐ＜０．０１）．缺血前静脉推注巯甲丙脯酸可以降低心肌晕厥时心肌局部ＡＮＧ－Ⅱ及ＮＥ的产生．结论：心肌局部肾素，ＡＮＧ－Ⅱ及ＮＥ在心肌晕厥的发病中具有重要意义，动物实验结果提示缺血前静脉应用巯甲丙脯酸防治可能是?
Objective: To investigate the role of renin, angiotensin Ⅱ (angiotensin Ⅱ) and norepinephrine (NE) in the pathogenesis of myocardial syncope and the effects of angiotensin converting enzyme inhibitor (ACE) captopril Myocardial ischemia - reperfusion injury whether has a protective effect. Methods: The rabbit model of myocardial syncope was established by ligation of coronary artery. The changes of renin, ANG-Ⅱ and NE in myocardium were detected by radioimmunoassay, and administered intravenously with captopril before ischemia. RESULTS: The local renin activity tended to increase after myocardial ischemia, and the local renin activity tended to increase after reperfusion. The renin activity [(609.3 ± 210) pg · mg-1 · H-1] was significantly higher than that of the control group [(196.4 ± 24.8) pg · mg-1 protein · h-1] (P <0.01). The content of ANG-Ⅱ in myocardium [(3005.1 ± 835.3) pg / mg protein] was significantly higher than that in the normal control group [(1535.4 ± 258.3) pg / mg protein] (P <0.01). Myocardial NE content [(3.0 ± 1.0) μg / g wet weight vs (1.18 ± 0.28) μg / g wet weight) was significantly higher (P <0.01). Pre-ischemic venous injection of captopril can reduce myocardial myocardial ANG-Ⅱ and NE production in patients with syncope. CONCLUSION: The renin, ANG-Ⅱ and NE in myocardium are important in the pathogenesis of myocardial syncope. Animal experiments suggest that the prevention and treatment of captopril in pre-ischemic vein may be?