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在蒙古沙鼠全脑缺血后呼吸100%的氧气会导致脂质过氧化增加和死亡率上升。

Breathing 100% oxygen after global brain ischemia in Mongolian Gerbils results in increased lipid peroxidation and increased mortality.

作者信息

Mickel H S, Vaishnav Y N, Kempski O, von Lubitz D, Weiss J F, Feuerstein G

出版信息

Stroke. 1987 Mar-Apr;18(2):426-30. doi: 10.1161/01.str.18.2.426.

DOI:10.1161/01.str.18.2.426
PMID:3564100
Abstract

Exposure of Mongolian gerbils to a 100% oxygen atmosphere after 15 minutes of global brain ischemia resulted in a marked increase in the production of pentane, an in vivo product of lipid peroxidation. Much less pentane production occurred in animals subjected to global brain ischemia then exposed to an air atmosphere and in animals exposed to a 100% oxygen atmosphere without ischemia. Gerbils placed in 100% oxygen for 3-6 hours after 15 minutes of ischemia also had a threefold increase in 14-day mortality compared with gerbils subjected to ischemia and then placed in an air atmosphere. These findings raise a serious question about the use of oxygen-enriched atmospheres during reperfusion following ischemia.

摘要

在全脑缺血15分钟后,将蒙古沙鼠暴露于100%氧气环境中,会导致戊烷生成显著增加,戊烷是脂质过氧化的一种体内产物。在经历全脑缺血后再暴露于空气环境的动物以及未经历缺血而暴露于100%氧气环境的动物中,戊烷生成量要少得多。缺血15分钟后置于100%氧气环境中3至6小时的沙鼠,与经历缺血后置于空气环境中的沙鼠相比,14天死亡率也增加了两倍。这些发现对缺血后再灌注期间使用富氧环境提出了严重质疑。

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