替米沙坦对慢性压力超负荷大鼠心肌细胞凋亡的干预作用  

Intervention of telmisartan to apoptosis of cardiomyocytes of chronic pressure overloaded rat

作　　者：周泉[1] 张同利[1] 吴大方[1] 

机构地区：[1]解放军第451医院心内科,陕西西安710054

出　　处：《第四军医大学学报》2008年第20期1855-1857,共3页Journal of the Fourth Military Medical University

摘　　要：目的:探讨大鼠腹主动脉缩窄法模拟慢性压力超负荷引起心肌肥大、细胞凋亡,给予替米沙坦干预后观察心肌细胞凋亡.方法:大鼠随机等分成3组,假手术组,腹主动脉缩窄组,替米沙坦+腹主动脉缩窄组,建立复制慢性超负荷增加引起心力衰竭大鼠模型,应用末端转移酶介导的缺口末端标记法(TUNEL)检测3组心肌细胞凋亡.结果:腹主动脉缩窄组,替米沙坦+腹主动脉缩窄组因慢性压力超负荷均引起心肌肥大、细胞凋亡,给予替米沙坦干预后,可以减少心肌细胞的凋亡(P<0.01).结论:腹主动脉缩窄法制备慢性压力超负荷大鼠心肌细胞凋亡,替米沙坦有明显的保护作用.AIM： To illustrate the rat abdominal aortic coarctation simulated chronic pressure overload caused myocardial hypertrophy and cell apoptosis and to observe the cardiomyocyte apoptosis after the intervention of telmisartan. METHODS： Rats were randomly divided into 3 groups ： sham-operation group, abdominal aortic coarctation group, telmisartan ＋ abdominal aortic coarctation group. Chronic heart failure model induced by an increase in load was established. Terminal transferase-mediated nick-end labeling （RUNEL） was used to detect the cardiomyocyte apoptosis in 3 groups. RESULTS： Cardiac hypertrophy and cell apoptosis were induced in abdominal aortic coarctation group and telmisartan ＋ abdominal aortic coarctation group due to chronic pressure overload. Telmisartan intervention significantly reduced myocardial apoptosis （ P 〈 0. 01 ）. CONCLUSION： Chronic pressure overloaded rat established by abdominal aortic coarctation displays cardiomyocyte apoptosis, and tehnisartan has protective effect.

关 键 词：大鼠 心肌/细胞学 细胞凋亡 替米沙坦 

分 类 号：R541[医药卫生—心血管疾病] R972[医药卫生—内科学]