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实验性兔蛛网膜下腔出血后，基底动脉壁丙二醛（ＭＤＡ）含量及超氧化物峻化酶（ＳＯＤ）、过氧化氢酶（ＣＡＴ）活性发生改变，基底动脉出现痉挛，应用ＳＯＤ后上述变化减轻。离体采用生物检定法发现，基底动脉受自由基损伤后，去甲肾上腺素（ＮＥ）诱导的血管收缩效应增强，而ＡＣｈ诱导的血管舒张效应减弱。用ＳＯＤ防止了ＡＣｈ诱导的血管舒张效应的减弱。结果表明，氧自由基参与了脑血管痉挛的发生，而脑血管受自由基损伤后，其内皮舒张因子释放减少是脑血管痉挛发病的重要因素。
After experimental rabbit subarachnoid hemorrhage, the contents of malondialdehyde (MDA) and the activities of superoxide dismutase (SOD) and catalase (CAT) in the basilar artery wall were changed, basilar artery spasm occurred. After application of SOD The above changes are alleviated. In vitro bioassay found that the basilar artery injury by free radicals, norepinephrine (NE) -induced vasoconstriction effect increased, while ACh induced vasodilatation effect weakened. Decreasing ACh-induced vasodilatation was prevented with SOD. The results showed that oxygen free radicals involved in the occurrence of cerebral vasospasm, and cerebrovascular injury by free radicals, the release of reduced release of endothelial relaxation factor is an important factor in the pathogenesis of cerebral vasospasm.