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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 cardiac dysfunction after open heart surgery, the exact pathogenesis has not yet been elucidated. In recent years, studies on the molecular level of cells show that the delayed recovery of myocardial glucose reperfusion leads to the accumulation of intracellular H +, and the enhancement of H + - Na + exchange leads to the overload of [Na +] i and the increase of Na + - Ca2 + Ca2 +] i overload, [Ca2 +] i overload and activation of Ca2-dependent protease cause partial selective degradation of troponin occurs, it is likely to be the key mechanism of myocardial stunning. These advances provide new theoretical and experimental evidence for further revealing myocardial stunning mechanisms.