压力超负荷致心肌肥大过程中心肌内分泌因子活化  

Endocrine Factors Activation of Rat Myocardium During Pressure Overload-induced Cardiac Hypertro-phy

作　　者：周小波[1] 苟小平 张艺[1] 缪书卉[1] 

机构地区：[1]第三军医大学新桥医院心内科,重庆400037 [2]上海市中冶医院内科

出　　处：《中国微循环》2004年第1期10-12,50,共4页Journal of Chinese Microcirculation

基　　金：国家自然科学基金资助(NO.39600041)

摘　　要：目的探讨急性压力超负荷心肌肥大的跨膜信号传递机制。方法分别利用放射免疫法、分光光度法、免疫组化及原位杂交法动态观察压力超负荷后大鼠心肌组织血管紧张素转换酶 (ACE)活性、血管紧张素Ⅱ(AngⅡ)、一氧化氮含量和碱性成纤维细胞生长因子(bFGF)表达的变化 ,并观察它们与压力超负荷心肌肥大的关系。结果随大鼠血压升高 ,心肌组织中ACE活性及AngⅡ含量均迅速升高(P<0.05) ,并持续保持高水平 ,bFGF表达先升高(P<0.05)后又恢复到正常水平 ;AngⅡ含量升高早于bFGF表达升高 ;而—氧化氮含量迅速降低并持续受抑(P<0.05)。结论心肌内分泌活化可能是介导压力超负荷致心肌肥大的重要机制。Objective To investigate the mechanism of mechanical signal transduction in cardiac hypertro-phy induced by pressure overload.Methods Changes of activity of angiotensin converting enzyme(ACE),concen-trations of angiotesinⅡ(AngⅡ),nitrite oxide(NO)and bFGF expression in rat myocardiumwere observed dynam-ically using radioimmunoassay,colorimetric method,immunohistochemisty and in situ hybridization,and their role in the pathogenesis of heart hypertrophy induced by pressure overload was also analyzed.Results Accompanying grad-ual elevation of pressure after abdominal aorta constriction,activity of ACE,concentration of AngⅡincreased rapid-ly,and kept at high level(P<0.05).Expression of bFGF was enhanced(P<0.05)at first and then was reduced to normal level,and its elevation was later than that of AngⅡ.However concentration of NO decreased immediately and kept at low level(P<0.05).Conclusions Heart hypertrophy induced by pressure overload may be mediated by myocardial endocrine activation.

关 键 词：压力超负荷 心肌肥大 内分泌学 

分 类 号：R542.2[医药卫生—心血管疾病]