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急性心肌梗塞时由于心肌的缺血缺氧和坏死,一方面使心肌线粒体机能受到抑制,通过机械与化学的作用,使高能磷酸键和ATP形成减少;另一方面促进心肌糖原分解和葡萄糖的摄取增加,产生过多的丙酮酸,从心肌释放乳酸。这些代谢障碍致使细胞膜泵作用失调,结果引起钠进入细胞内,钾逸出,而极化溶液(GIK)则可逆转上述这些病理生理变化。
Acute myocardial infarction due to myocardial ischemia hypoxia and necrosis, on the one hand myocardial mitochondrial function is inhibited by mechanical and chemical effects, so that high-energy phosphate bonds and ATP formation decreased; the other hand, promote myocardial glycogenolysis and glucose Increased intake, resulting in excessive pyruvate, release of lactic acid from the myocardium. These metabolic disorders cause dysregulation of the membrane pump, which causes sodium to enter the cell and potassium escape, whereas the polarized solution (GIK) reverses these pathophysiological changes.