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出血性休克时,细胞膜去极化、细胞内钠和水积聚,细胞外钾增加,提示细胞膜破裂,钠钾 ATP 酶泵失去作用。而细胞内能量贮备耗尽和 ATP 依赖性细胞反应的抑制,可能是由于出血性休克期间细胞膜转运功能改变所致。休克时静脉给予三磷酸腺苷一氯化镁(ATP-MgCl_2),可使心脏充盈度、心排出量和心脏作功增加,提高区域性灌注和改善细胞的代谢。
Hemorrhagic shock, the cell membrane depolarization, intracellular accumulation of sodium and water, extracellular potassium increased, suggesting that cell membrane rupture, sodium potassium ATPase pump lost effect. The depletion of intracellular energy stores and the inhibition of ATP-dependent cellular responses may be due to altered cell membrane transport functions during hemorrhagic shock. Intravenous administration of adenosine triphosphate-magnesium chloride (ATP-MgCl 2) during shock can increase cardiac filling, cardiac output and cardiac work, improve regional perfusion and improve cellular metabolism.