脑缺血再灌注对大鼠不同脑区丙二醛、谷胱甘肽含量及谷胱甘肽过氧化物酶活性的影响

目的：探讨脑缺血再灌注时自由基代谢变化在迟发性神经元损伤中作用。方法：采用闭塞大鼠４条动脉全脑缺血模型，在全脑缺血３０分钟和缺血后再灌注不同时间，分别观察某些脑区丙二醛（ＭＤＡ）、谷胱甘肽（ＧＳＨ）含量以及谷胱甘肽过氧化物酶（ＧＳＨＰｘ）活性变化。结果：在大脑皮层和海马中，缺血３０分钟后，ＧＳＨ、ＧＳＨＰｘ显著下降，细胞膜ＭＤＡ有所增加，但无显著性差异。随再灌注时间延长，胞浆中ＧＳＨ逐渐回升，而ＧＳＨＰｘ进一步下降，并且细胞膜ＭＤＡ显著升高。在丘脑和下丘脑，各组ＧＳＨ、ＭＤＡ变化均无显著性差异，ＧＳＨＰｘ变化则与大脑皮层和海马中相似，但下降幅度较小。结论：脑缺血引发的自由基损伤主要发生在缺血再灌注期，且海马是脑缺血再灌注损伤中最易损伤区。

The effects of ischemia reperfusion on malondialdehyde and glutathione contents and glutathione peroxidase activity in different regions of rat brain/

Objective:To investigate the changes of free radical metabolism in cerebral ischemiareperfusion.Methods:By a rat cerebral ischemic model with four vessels occlusion,to observe the changes of malondialdehyde(MDA) and glutathione (GSH) contents and glutathione peroxidase(GSHPx) activity after 30 minutes ischemia and in different reperfusion time.Results:In the cerebral cortex and hippocampus,the GSH content and GSHPx activity were declined significantly and the level of MDA was elevated but no significant difference following 30 minutes ischemia as compared with the control.When reperfusion was prolonged after 30 minutes ischemia,the GSH content was gradually raised,but the GSHPx activity presented a continuative decline and the level of MDA in the cerebrocellular membranes was enhanced markedly.These changes were significant in the cerebral cortex and hippocampus,but were no significant or within a narrow range in thalamus and hypothalamus.Conclusions:These data suggested that the free radical injury induced by the cerebral ischemia mainly occurred during ischemiareperfusion and hippocampus was the most vulnerable area in the region of brain.