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乙醇对实验性失血性休克中乳酸酸中毒的影响。

Effect of ethanol on lactic acidosis in experimental hemorrhagic shock.

作者信息

Garrison H G, Hansen A R, Cross R E, Proctor H J

出版信息

Ann Emerg Med. 1984 Jan;13(1):26-9. doi: 10.1016/s0196-0644(84)80379-0.

Abstract

Many trauma victims who have hemorrhagic shock are also intoxicated. Ethanol could worsen the severity of shock and decrease the amount of blood loss necessary to reach or maintain the shock state, perhaps by increasing lactic acidosis. We examined the effect of ethanol on lactic acidosis in a group of rats that were intoxicated, then put in a state of hemorrhagic shock (MAP = 40 mm Hg). These animals were compared to a control group that were in a similar state of hemorrhagic shock but not intoxicated. The volumes of blood necessary to reach and maintain the predetermined model state of shock for two hours in each group were also measured. The animals were paralyzed and placed on controlled ventilation. The ethanol produced an expected baseline lactic acidosis, and it took significantly less blood volume loss to keep the intoxicated group in shock. However, during shock there was no significant difference in the state of lactic acidosis. These results suggest that acute ethanol intoxication made the animals more sensitive to hemorrhage. This effect was not mediated by an increase in lactic acidosis in our model.

摘要

许多患有失血性休克的创伤患者同时也处于醉酒状态。乙醇可能会加重休克的严重程度,并减少达到或维持休克状态所需的失血量,这可能是通过增加乳酸酸中毒来实现的。我们研究了乙醇对一组已醉酒、随后进入失血性休克状态(平均动脉压 = 40 mmHg)大鼠的乳酸酸中毒的影响。将这些动物与处于类似失血性休克状态但未醉酒的对照组进行比较。还测量了每组达到并维持预定休克模型状态两小时所需的血量。动物被麻痹并进行控制通气。乙醇产生了预期的基线乳酸酸中毒,并且使醉酒组维持休克状态所需的失血量显著减少。然而,在休克期间,乳酸酸中毒状态没有显著差异。这些结果表明,急性乙醇中毒使动物对出血更敏感。在我们的模型中,这种效应不是由乳酸酸中毒的增加介导的。

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