【摘要】 目的 观察伊贝沙坦和咪哒普利在自发性高血压大鼠（SHR）心肌肥厚逆转过程中细胞凋亡的变化,探讨其可能机制与意义。方法 选13周龄SHR 30只,随机均分为3组,即伊贝沙坦治疗组（SHR-I组）、咪哒普利治疗组（SHR-M组）和非治疗对照组（SHR组）,另设同源正常血压大鼠10只（WKY组）作为对照。饲养13周后,伊贝沙坦组大鼠服用伊贝沙坦50mg·kg^-1·d^-1,咪哒普利组服用咪哒普利3mg·kg^-1·d^-1,治疗15周,每2周测血压、体重1次,治疗结束时称左心室重量,放免法检测血浆和心肌血管紧张素Ⅱ（Aug Ⅱ）浓度。应用末端脱氧核糖核苷酸转移酶介导的带荧光的dUTP缺口末端原位标记法（Tunel）检测各组大鼠左室心肌细胞凋亡的变化。结果（1）28周时,SHR组血压、左室重量指数〔（3.56±0.38）×10^-3〕、心肌细胞横径[（17.38±1.21）μm]、血浆和心肌AugⅡ[分别为（387.72±26.21）pg/ml、（16.83±2.72）ng/g]均高于 WKY组（P<0.05）,SHR-Ⅰ组和SHR-M组血压、左室重量指数[（2.57±0.43）×10^-3、（2.49±0.36）×10^-3]、心肌细胞横径[（14.24±0.83）、（13.79±0.77）μm]明显低于SHR组（P<0.01）,SHR-I组血浆和心肌AngⅡ[（681.12±34.48）、（28.51±3.62）ng/g]显著高于SHR组（P < 0.01）,SHR-M组血浆和心肌AugⅡ低于SHR组（P<0.01）;（2）与SHR组更多还原

【Abstract】 Objective To explore the changes of cardiomyocytes apoptosis in the effect of irhesartan and imidapril on regressing cardiac hypertrophy in spontaneous hypertensive rat (SHR), and its mechanism. Methods Thirty 13-week-old SHR were randomly divided into three groups: SHR positive control group, irhesartan treated group(50 mg ·kg-1 ·day -1 ) , imidapril treated group(3 mg ·kg -1 ·day-1 ), and normotensive Wistar-Kyoto rats(WKY) as controls. Blood pressure of rats were monitored periodically. After 15 weeks, all rats were killed and left ventricle weight(LVW) were measured, plasma and myocardium angiotensin Ⅱ concentrations were examined by radioimmunoassay. Then the changes of cardiomyocytes apoptosis using in situ TDT-mediated dUTP nick end labeling(Tunel) were studied. Results Blood pressure, LVW, AngⅡ level of plasma and left ventricle were higher in SHR than those in WKY(P<0. 05). Compared with WKY, the apoptosis of untreated SHR was increased ( P < 0. 01). Both irbesartan and imidapril administrations were associated with the normalization of apoptosis, but imidapril was more effective ( P < 0. 05 ). Conclusions The chronic administration of irbesartan and imidapril normalizes the apoptosis index in the left ventricle of SHR, and it is independent of its hemocdynamic effect. Ang Ⅱ may play a key role in the heart remodeling by inducing apoptosis.更多还原