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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
Objective To investigate the changes of apoptosis of irbesartan and imidapril in the course of cardiac hypertrophy in spontaneously hypertensive rats (SHR) and to explore its possible mechanism and significance. Methods Thirty SHRs of 13 weeks old were randomly divided into 3 groups: SHR-I group, SHR-M group and SHR group ), Another set of 10 rats with normal normotensive (WKY group) as a control. After 13 weeks of feeding, the rats in irbesartan group were treated with 50 mg · kg -1 d · -1 of irbesartan, 3 mg · kg -1 of imidapril in the imidapril group ) · D ~ (-1) for 15 weeks. Blood pressure and weight were measured every 2 weeks. Left ventricular weight was measured at the end of treatment. Plasma and myocardial angiotensin Ⅱ (Ⅱ) concentrations were measured by radioimmunoassay. End-to-end deoxyribonucleotide transferase-mediated dUTP nick end labeling (Tunel) was used to detect the changes of left ventricular myocytes apoptosis. Results (1) At 28 weeks, the blood pressure, left ventricular mass index (3.56 ± 0.38) × 10 -3, heart diameter [(17.38 ± 1.21) μm], plasma and cardiac augⅡ (P <0.05). The blood pressure, LV mass index (2.57 ± 0.43, P <0.05) in SHR-Ⅰ group and SHR-M group were significantly higher than those in WKY group (387.72 ± 26.21 pg / ml and 16.83 ± 2.72 ng / (14.24 ± 0.83), (13.79 ± 0.77) μm] were significantly lower than those in SHR group (P <0.01) ) In SHR-I group were significantly higher than those in SHR group (P <0.01), but Ang II in plasma and myocardium in SHR-I group was significantly lower than that in SHR group [(681.12 ± 34.48), (28.51 ± 3.62) ng / P <0.01); (2) and SHR group