摘要
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。
Abstract In this paper, we made the model for forebrain ischemia and reperfution in Wistar rats by four-vessel occlusion. The levels of LPO, SOD and GSH-Px were determined in several brain regions,including hippocampus, neocortex, striatum, thalamus and cerebellum for 6 hours-7 days after postischemic reperfusion. The results showed that levels of LPO increased on 6h-5d(p<0.01, p<0.05) in all regions above, SOD decreased after reperfusion until fifth day in hippocampus, thalamus and striatum, but not increased to controled level at 7 day in neocortex and cerebellum (p<0. 01),and GSH-Px revealed double phases, i. e. decreasing within 24 hours and then increasing to top at 48 hours in all regions. There was negative correlation between the levels of LPO and SOD, but there was no relationship between LPO and GSH-Px. We also discussed the role of free radicals on delayed neuronal death.
出处
《中风与神经疾病杂志》
CSCD
北大核心
1994年第3期129-132,共4页
Journal of Apoplexy and Nervous Diseases
基金
国家自然科学基金
