心肌顿抑的细胞分子机制研究进展  

Advances in Research of Molecular and Cellular Mechanisms of Myocardial Stunning

作　　者：隋东虎[1] 石应康[1] 

机构地区：[1]华西医科大学附属第一医院胸心外科,成都610041

出　　处：《中国胸心血管外科临床杂志》2000年第3期183-186,共4页Chinese Journal of Clinical Thoracic and Cardiovascular Surgery

摘　　要：心肌顿抑是心脏直视手术后心功能障碍的主要病理基础 ,其确切发病机制至今尚未阐明。近年来细胞分子水平的研究表明 ,缺血再灌注后心肌葡萄糖氧化延迟恢复引起细胞内 H+ 聚积 ,H+ - Na+ 交换增强致使 [Na+ ]i 超负荷 ,进而 Na+ - Ca2 + 交换增强导致一过性 [Ca2 + ]i 超负荷 ,[Ca2 + ]i 超负荷又可激活 Ca2 + 依赖性蛋白酶引起肌钙蛋白 发生部分选择性降解 ,很可能是造成心肌顿抑的关键机制。这些研究进展为进一步揭示心肌顿抑机制提供了新的理论和实验依据。Myocardial stunning is the main pathological basis of heart dysfunction after open heart operation, its exact pathogenesis hasn't been clarified until today.In recent years,the molecular and cellular studies have revealed possibly crucial pathogenesis of myocardial stunning that delayed recovery of myocardial glucose oxidation causes intracellular H + accumulation which augments H + Na + exchange thus leading to [Na +] i overload.[Na +] i overload increases Na + Ca 2+ exchange resulting in transient [Ca 2+ ] i overload,which may activate Ca 2+ dependent protease causing partial selective troponin I degradation of myofibris after myocardial ischemia and reperfusion.These progresses provide new theoretic and experimental evidence for further elucidating the pathogenesis of myocardial stunning.

关 键 词：心肌顿抑 钙离子 肌钙蛋白 心脏直视术 

分 类 号：R346[医药卫生—基础医学]