急性压力超负荷诱导心肌内分泌活化  

Endocrine activation of rat heart stimulated by pressure overload

作　　者：冯兵[1] 陈意生[2] 何作云[3] 黄敏[3] 周晓波[3] 

机构地区：[1]军事医学科学院放射医学研究所病理研究室,北京100850 [2]第三军医大学病理学教研室 [3]第三军医大学新桥医院心内科,重庆400037

出　　处：《中国病理生理杂志》1999年第10期891-893,共3页Chinese Journal of Pathophysiology

基　　金：国家自然科学基金!39600041

摘　　要：目的：探讨压力超负荷致心肌肥大的跨膜信号传递机制。方法：利用放射免疫法及分光光度法动态观察压力超负荷后大鼠心肌组织血管紧张素转换角活性，血管紧张素Ⅱ、内皮索和一氧化氢含量的变化，并观察它们与压力超负荷心肌肥大的关系。结果：随大鼠动脉血压逐步升高，心肌组织中血管紧张素转换酶活性，血管紧张素Ⅱ、内皮素含量均迅速升高（P＜0．05），并持续保持高水平，血管紧张素Ⅱ升高早于内皮系，而一氧化氛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。To investigate the mechamsm of mechanical signal transmembrane transduction in heart hypertrophyinduced by pressure overload. METHODS: Changes of angactivity 0f angiotnsin conveIting enZyme(ACE), concentrachons ofangiotensin II (Ang II) and endothelin - l (ET) and nitrite oxide (NO) in rat hearts were obserVed dynthecally using ra-dio~ and co^tric methed, and itS r0e in the Pathognnesis 0f he8xt hyPeItIDPhy induced by pressure overloadwas also analyzed.RESULTS:Accompanyed gradtion of arterial pressure after abdominal aorta constriction, ac-tivity of ACE, concentration of Ang II and ET increased rapidly,and kept at high level (P < 0.05), the elevation of AngII was earlier than that of ET. Howevr, concentration of NO decreased ediately and kept at low level (P < 0. O5).C0NCLUSION: Heart hypertrophy induced by pressure overload may be mediated by myocardial myocardial endocrine activation.

关 键 词：压力 心肌病 内分泌学 心肌肥大 

分 类 号：R542.202[医药卫生—心血管疾病]