压力超负荷性心肌肥厚发病机制的研究  

Study of Mechanism of Pressure Overload-Induced Myocardial Hypertrophy in Rats

作　　者：张利军[1] 魏蕾[1] 徐怡[1] 

机构地区：[1]武汉大学医学院病理生理学教研室,邮政编码武汉430071

出　　处：《微循环学杂志》2005年第3期19-21,F0005,F0007,F0008,共6页Chinese Journal of Microcirculation

基　　金：湖北省卫生厅基金资助(JX1B165)

摘　　要：目的:探讨α1、β受体阻断剂派唑嗪(Prazosin,Pra)、心得安(Propra-nolol,Pro)及钙离子拮抗剂尼群地平(Nitrendipine,Nit)在压力超负荷性心肌肥厚发病学中的意义。方法:采用Pra、Pro和Nit治疗大鼠腹主动脉缩窄所致左室肥厚(LVH)。结果:Pra和Nit能抑制早期肥厚心肌c-fosmRNA表达,6周后Pra组和Nit组较LVH组之BP,LVW/BW均显著下降,同时心脏舒张功能改善,Na+-K+ATPase活性增强;而Pro不能有效改善LVH。结论:Pra和Nit治疗成功预防了心肌肥厚的发生,而Pro不能。提示儿茶酚胺参与压力超负荷性心肌肥厚的形成,其效应不仅涉及后负荷的高低,也可通过α1肾上腺素能受体而不是β肾上腺素能受体对心肌产生直接性致肥大作用,同时钙离子可作为第二信使参与引起心肌细胞肥大的信息传递。Objective： To study the roles of Pra （Prazosin）, Pro （Propranolol） and Nit （Nitrendipine） in pressure overload-induced myocardial hypertrophy in rats. Method： Rats with left ventricular hypertrophy （LVH） induced by abdominal aorta constriction were treated with Pra, Pro and Nit respectively. Results： Pra and Nit inhibit increasing of c-fos mRNA level in the early stage of pressure overload-induced myocardial hypertrophy. 6 weeks after operation, in the Pra group and the Nit group, blood pressure, left ventricular weight/body weight （LVW/BW） significantly decreased, while the diastolic function of the left ventricle improved and the activity of Na^＋ -K^＋ ATPase markedly increased. Pro can＇t inhibit the development of LVH effectively. Conclusion： Pra and Nit but not Pro can successfully prevent the development of LVH. It＇s implicated that catecholamine is involved in the development of pressure overload-induced myocardial hypertrophy. And catecholamine can not only affect the afterload, but also have the direct effect on myocardial hypertrophy through α1-adrenergic receptors but not β-adrenergic receptors. In addition, Ca^2＋ as a second messenger is involved in the signal transduction that caused pressure overload-induced myocardial hypertrophy.

关 键 词：压力超负荷性心肌肥厚 发病机制 压力超负荷性左室肥厚 腹主动脉缩窄法 心肌肥厚模型 Β受体阻断剂 钙离子拮抗剂 心肌细胞肥大 尼群地平 

分 类 号：R542.2[医药卫生—心血管疾病] R541-33[医药卫生—内科学]