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低压缺氧及吡拉西坦治疗后大鼠脑线粒体的呼吸功能

Respiratory function of rat brain mitochondria after hypobaric hypoxia and piracetam treatment.

作者信息

Wustmann C, Petzold D, Kunz W, Fischer H D

机构信息

Institute of Pharmacology and Toxicology, Medical Academy, Carl Gustav Carus, Dresden, GDR.

出版信息

Biomed Biochim Acta. 1987;46(7):635-8.

PMID:3426574
Abstract

After an acute hypobaric hypoxia the mitochondrial respiratory control index is reduced in consequence of a decreased active-state respiration. The finding is paralleled by decreased uncoupled respiration and a not significantly changed resting-state respiration. Long term hypoxic exposures show adaptive traits of this criterion of mitochondrial energy metabolism. The antihypoxic effect of piracetam may be reflected in a delayed normothermic in vitro aging of mitochondrial suspension.

摘要

急性低压缺氧后,由于活性状态呼吸减少,线粒体呼吸控制指数降低。这一发现伴随着解偶联呼吸减少和静息状态呼吸无显著变化。长期低氧暴露显示出线粒体能量代谢这一标准的适应性特征。吡拉西坦的抗缺氧作用可能反映在线粒体悬液的体外正常体温老化延迟上。

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