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[急性肝缺血时能量生成紊乱的机制]

[Mechanism of disorders in energy formation in acute hepatic ischemia].

作者信息

Levandovskiĭ I V, Liakhovich V V, Panov A V, Solov'ev V N, Tsyrlov I B

出版信息

Biull Eksp Biol Med. 1977 Sep;84(9):301-3.

PMID:199293
Abstract

Respiration of hepatic mitochondria of rats after addition of ischemic toxin to the incubation medium was compared with respiration of mitochondria isolated from an ischemic rat liver. Its change could be prevented in both cases by the preliminary administration of dithiotreitol and could be decreased by the subsequent addition of cytochrome C or dithiotreitol into the incubation medium. Similarity of the mechanisms of disturbed energy formation in vivo and in vitro is supposed.

摘要

将缺血毒素添加到孵育介质后,大鼠肝脏线粒体的呼吸作用与从缺血大鼠肝脏分离的线粒体的呼吸作用进行了比较。在这两种情况下,预先给予二硫苏糖醇可防止其变化,随后向孵育介质中添加细胞色素C或二硫苏糖醇可使其降低。推测体内和体外能量形成紊乱机制具有相似性。

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1
[Mechanism of disorders in energy formation in acute hepatic ischemia].[急性肝缺血时能量生成紊乱的机制]
Biull Eksp Biol Med. 1977 Sep;84(9):301-3.
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[Characteristics of the intracellular action of ischemic toxin].[缺血毒素的细胞内作用特征]
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Effect of free fatty acids on hepatic adenine nucleotide content and oxidative metabolism.
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Phosphoenolpyruvate prevents the decline in hepatic ATP and energy charge after ischemia and reperfusion injury in rats.磷酸烯醇丙酮酸可防止大鼠缺血再灌注损伤后肝ATP和能荷的下降。
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