[gaba能药物对创伤性水肿脑线粒体氧化磷酸化的影响]。

Farmakologiia i toksikologiia Pub Date : 1991-11-01
V E Novikov, A n Sharov
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引用次数: 0

摘要

用极谱法研究了大鼠脑创伤性水肿过程中线粒体氧化磷酸化的动态变化。结果发现,损伤后24小时线粒体氧化速率降低,呼吸链的结合度代偿性增加。吡拉西坦(1g /kg)、苯乙酯(50mg /kg)和氧丁酸钠(0.2 g/kg)在较小程度上阻止了线粒体在脑创伤性水肿发展过程中的变化,并增强了线粒体的代偿能力。
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[The effect of GABA-ergic agents on oxidative phosphorylation in the brain mitochondria in traumatic edema].

The condition of oxidative phosphorylation in the rat brain mitochondria was studied polarographically in dynamics of the brain traumatic edema. It was found that 24 hours after the trauma the rate of oxidation in mitochondria decreased and the degree of conjugation in the respiratory chain compensatorily increased. Piracetam (1 g/kg), phenibut (50 mg/kg) and to a lesser degree sodium oxybutyrate (0.2 g/kg) prevented the 'changes and enhanced the compensatory capacities of mitochondria during the development of traumatic edema of the brain.

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