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本文采用四血管阻断方法制成Ｗｉｓｔａｒ大鼠全脑缺血１０分钟再灌流模型。分别于再灌流７天内对新皮层、海马、丘脑、纹状体和小脑等五个脑区的ＬＰＯ、ＳＯＤ、ＧＳＨ—Ｐｘ含量进行测定。ＬＰＯ在各脑区于再灌流后开始升高，２４小时达高峰，第５天基本降至对照组水平。ＳＯＤ在６小时内迅速降至最低水平，然后逐渐回升，但在第７天时仍低于对照水平。ＧＳＨ—Ｐｘ在各脑区均呈双时相改变，先降后升，然后再逐渐下降，在第７天时略低于对照组。经相关分析，ＬＰＯ与ＳＯＤ呈显著负相关，ＬＰＯ与ＧＳＨ—Ｐｘ无相关关系。本文还对自由基在脑缺血后迟发性神经元坏死中的作用机制进行了讨论。
In this paper, four-vessel occlusion method was used to make Wistar rat model of global ischemia reperfusion 10 minutes. The contents of LPO, SOD and GSH-Px in five brain regions including neocortex, thalamus, thalamus, striatum and cerebellum were measured respectively within 7 days after reperfusion. LPO in each brain area began to rise after reperfusion, peaked at 24 hours, basically dropped to the control level on the 5th day. SOD dropped rapidly to its lowest level within 6 hours and then gradually rose but remained below control levels on day 7. GSH-Px in both brain regions showed a dual phase change, first decreased and then increased, and then gradually decreased, slightly lower than the control group on the 7th day. Correlation analysis showed that there was a significant negative correlation between LPO and SOD and no correlation between LPO and GSH-Px. This article also discusses the mechanism of free radicals in the delayed neuronal necrosis after cerebral ischemia.