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以脑缺血为模型研究γ-羟基丁酸锂抗缺氧作用机制

[Study of the mechanism of the anti-hypoxic action of lithium oxybutyrate using cerebral ischemia as a model].

作者信息

Ivanova I A, Bobkov Iu G, Losev A S

出版信息

Biull Eksp Biol Med. 1985 Sep;100(9):319-22.

PMID:4041599
Abstract

A study was made of energy metabolism and concentration of malonic dialdehyde (MDA) in cerebral tissue of mice given sodium hydroxybutyrate and lithium hydroxybutyrate 30 and 60 s after decapitation. Administration of lithium hydroxybutyrate brought about a more economic consumption of the glycogen pool as compared with "hypoxic" control. The differences were revealed in the action of both salts on ATP. The concentration of MDA declined after their administration, lithium hydroxybutyrate being more efficacious. The possible mechanisms of the action of lithium hydroxybutyrate are discussed.

摘要

对断头后30秒和60秒给予羟基丁酸钠和羟基丁酸锂的小鼠脑组织中的能量代谢和丙二醛(MDA)浓度进行了研究。与“缺氧”对照组相比,给予羟基丁酸锂使糖原池的消耗更经济。两种盐对三磷酸腺苷(ATP)的作用存在差异。给药后丙二醛浓度下降,羟基丁酸锂更有效。文中讨论了羟基丁酸锂作用的可能机制。

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