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脂质过氧化在内脏缺血性休克发病机制中的作用

[Role of lipid peroxidation in pathogenesis of visceral ischemic shock].

作者信息

Shneĭvaĭs V B, Amilov K S

出版信息

Vopr Med Khim. 1991 May-Jun;37(3):33-5.

PMID:1949680
Abstract

Patterns of lipid peroxidation, chemoluminescence and antiradical activity of rat blood serum were studied after simulation of visceral-ischemic shock developed as a result of two-hour-long ischemia of the small intestines and of right-side part of large intestine. Toxic effects of oxygen, accompanied by considerable activation of lipid peroxidation, were of importance in pathogenesis of this shock. Accumulation of lipid peroxidation products in blood occurred at the step of the intestine ischemia and was distinctly increased after restoration of circulation in the tissue. Increased inhibition of blood serum chemoluminescence as well as elevation of lipid antiradical activity were observed depending on steps of the shock development.

摘要

在模拟因小肠和大肠右侧两小时缺血而引发的内脏缺血性休克后,对大鼠血清中的脂质过氧化、化学发光和抗自由基活性模式进行了研究。氧的毒性作用伴随着脂质过氧化的显著激活,在这种休克的发病机制中具有重要意义。脂质过氧化产物在肠道缺血阶段在血液中积累,并且在组织循环恢复后明显增加。根据休克发展的阶段,观察到血清化学发光抑制增加以及脂质抗自由基活性升高。

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