自由基与兴奋性氨基酸在反复性脑缺血神经元损伤中的作用

EFFECT OF FREE RADICALS AND EXCITATORY AMINO ACIDS IN NEURONAL IN- JURIES FOLLOWING REPEATED CEREBRAL ISCHEMIA

对比研究了单次１５ｍｉｎ和３Ｘ５ｍｉｎ大鼠全脑缺血再灌流及ＮＭＤＡ受体拮抗剂ＭＫ－８０１治疗后脑组织超氧化物歧化酶（ＳＯＤ）、丙二醛（ＭＤＡ）的活性和含量变化及相应病理改变。发现反复缺血及其再灌流早期皮层、海马ＳＯＤ活性显著降低，ＭＤＡ含量延迟性持续增高，神经元损害显著重于单次缺血组；ＭＫ－８０１能显著升高ＳＯＤ活性，降低ＭＤＡ含量，同时明显改善神经元组织病理损害。提示兴奋性氨基酸和自由基可能参与反复性脑缺血神经元损害的病理机制，二者间亦存在着相互作用。

Malondialdehyde(MDA content, superoxide dismutase (SOD) activity and pathologicalchanges in rat brain were studied during global ischemid, of a single 15-minute period and three repeated 5-minute periods at hourly intervals respectively。 Both cases were followed by perfusion。 The effect of MK-801, a NMDA receptor antagonist was also examined. SOD activity in neocortex and hippocampus in therepeated ischemic group decreased significantly during ischemia and early reperfusion, while delayed per-sistent increase was found in the content of MDA, and neuronal injuries were found to be more severe inthe group of repeated cerebral ischemia than those in the single ischemic insult group. MK-80l is effectivenot only in increasing SOD activity, but also in decreasing the content of MDA and in ameliorating thehistopathological damages of neurons. It suggests that excitatory amino acids and free radicals may be in-volved in the pathogenesis of repeated cerebral ischmic damage, and interaction may occur between thesetwo mediators.