血管紧张素转换酶2激活／血管紧张素转换酶抑制预防肺动脉高压右心衰竭的作用及机制研究  

Effect and mechanisms of angiotensin converting enzyme 2 activation/angiotensin converting enzyme inhibition in prevention of right heart failure in pulmonary artery hypertension

作　　者：陈梦娜[1] 聂美玲 邹晓昭 郭雯[1] 赵铁夫[1] 杜小兵[1] 田蕾[1] 马涵英[1] 

机构地区：[1]首都医科大学附属北京安贞医院心内科,100029

出　　处：《中国医药》2017年第5期698-702,共5页China Medicine

基　　金：国家自然科学基金（81200179）;北京市卫生系统高层次卫生技术人才培养计划（2013-3-004）;高等学校博士学科点专项科研基金资助课题（20111107120021）

摘　　要：目的探究激活血管紧张素转换酶2（ACE2）、抑制ACE对肺动脉高压（PAH）右心衰竭的预防作用及机制。方法选取体质量240—260g雄性sD大鼠33只，完全随机分为空白对照组（n=6）、PAH右心衰竭组（n=9）、ACE2激动剂（Res）干预组（n=9）、ACE抑制剂（ACEI）干预组（n=9），饲养6周后，测定各组大鼠心肺功能，血浆、右心室心肌及肺组织中血管紧张素Ⅱ（AngⅡ）、Ang（1-7）水平，右心室心肌及肺组织中ACE、ACE2、血管紧张素1型受体（AT，R）、Mas蛋白表达。结果与PAH右心衰竭组相比，饲养6周时，Res及ACEI干预组肺动脉血流加速时间，右心室射血分数、缩短分数明显增加（均P〈0．05）。与PAH右心衰竭组比较，Res及ACEI干预组血浆、右心室心肌及肺组织中AngⅡ／Ang（1-7）比值均明显降低，右心室心肌ACE2蛋白表达明显增加，ACE、AT，R蛋白表达明显减少（均P〈0．05），而肺组织各组ACE、ACE2、AT，R、Mas蛋白表达差异均无统计学意义（均P〉0．05）。结论ACE2激活／ACE抑制可调控PAH右心衰竭时肾素-血管紧张素系统失衡，以右心室局部作用为主。Objective To investigate the effect and mechanisms of angiotensin converting enzyme（ACE）2 activation and ACE inhibition in prevention of pulmonary artery hypertension （PAH） induced right heart failure. Methods Thirty-three male SD rats were randomly assigned into blank control group （ n = 6 ） , PAH induced fight heart failure group （ n = 9 ）, ACE2 agonist （Res） intervention group （ n = 9 ） and ACE inhibitor （ACEI） intervention group（ n =9）. After feeding 6 months, cardio pulmonary function indexes were determined; levels of angiotensin Ⅱ （Ang Ⅱ） and Ang（1-7） in plasma, myocardium of right ventricle and lung tissue were detected; levels of ACE, ACE2, angiotensin type 1 receptor（ AT1R） and Mas protein in myocardium of fight ventricle and lung tissue were detected. Results Pulmonary artery flow acceleration time, fight ventricular ejection fraction （RVEF） and right ventricular fractional shortening（RVFS） in Res intervention group and ACEI intervention group were significantly higher than those in PAH induced fight heart failure group（P 〈 0. 05 ）. Ratios of AngⅡ/Ang （1-7） in plasma, myoeardium of right ventricle and lung tissue in Res intervention group and ACEI intervention group were significantly lower than those in PAH induced right heart failure group（P 〈0. 05）. Levels of ACE2 in myocardium of right ventricle in Res intervention group and ACEI intervention group were significantly higher and ACE, AT1R were significantly lower than those in PAH induced right heart failure group（P 〈0. 05） ; ACE, ACE2, ATIR and Mas protein in lung tissue had no significant differences among groups（P 〈0. 05）. Conclusion ACE2 activation/ACE inhibition can regulate the renin angiotensin system in PAH induced right heart failure in rats; the local effect on right ventricle is more obvious.

关 键 词：高血压 肺性 心力衰竭 血管紧张素转换酶2 血管紧张素转换酶抑制药 

分 类 号：R54[医药卫生—心血管疾病]