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大鼠脑不完全缺血后再灌注期间脂质过氧化的时间进程。

Time course of lipid peroxidation during incomplete ischaemia followed by reperfusion in rat brain.

作者信息

Horáková L, Lukovic L, Uraz V, Stolc S

机构信息

Institute of Experimental Pharmacology, Slovak Academy of Sciences, Bratislava.

出版信息

Physiol Bohemoslov. 1990;39(6):513-7.

PMID:2103637
Abstract

The time course of lipid peroxidation was studied in the rat brain cortex after ischaemia and reperfusion. The ischaemia was induced by 4-hour occlusion of both common carotid arteries and was followed by reperfusion of different duration (10, 30 or 60 min). The extent of lipid peroxidation was determined by measurement of conjugated dienes (CD) and TBA reactive products. Maximal values of CD and TBA reactive products were found after 10- and 30-minute reperfusion. This indicated the most suitable time interval for studying the effect of antioxidants and oxygen radical scavengers in this model of brain ischaemia.

摘要

研究了大鼠脑皮质缺血再灌注后脂质过氧化的时间进程。通过双侧颈总动脉闭塞4小时诱导缺血,随后进行不同时长(10、30或60分钟)的再灌注。通过测量共轭二烯(CD)和硫代巴比妥酸反应产物来确定脂质过氧化的程度。在再灌注10分钟和30分钟后发现CD和硫代巴比妥酸反应产物的最大值。这表明在该脑缺血模型中研究抗氧化剂和氧自由基清除剂作用的最合适时间间隔。

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Time course of lipid peroxidation during incomplete ischaemia followed by reperfusion in rat brain.大鼠脑不完全缺血后再灌注期间脂质过氧化的时间进程。
Physiol Bohemoslov. 1990;39(6):513-7.
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Ischemia/Reperfusion-induced oxidative stress causes structural changes of brain membrane proteins and lipids.缺血/再灌注诱导的氧化应激会导致脑膜蛋白和脂质的结构变化。
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引用本文的文献

1
Short cerebral ischemia and subsequent reperfusion and treatment with stobadine.
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