内皮舒张因子与氧自由基在脑血管痉挛发病中的作用

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。

THE ROLE OF ENDOTHELIUM DERIVED RELAXING FACTOR AND OXYGEN FREER RADICALIN PATHOGENESIS 0F CEREBRAL VASO

In experimental SAH,the MDA content was increased and activitics of SOD,CAT were de-creased in the wall of rabbit basilar arteries and angiography. showed a significant contraction ofbasilar artery. These changes were attenuated by treatment with SOD. In vitro,the relaxation ofbioassay rings induced by ACh was reduced and the con traction induced by NE was markedlyaugmented by free radical injury of the basilar artery. Electronmicroscopy showed that the intimaof basilar artery was damaged by free radical.Pretreatment with SOD prevented the decrease inrelaxation of bioassay rings induced by ACh and attenuated the lesions of endothelium in thebasilar arteries. These results suggest that oxygen free radical plays a key role in cerebralvasospasm and the reduction of EDRF release after the basilar artery was injured by free radicalmight be involved in the pathogenesis of cerebral vasospasm following subarachnoid hemorrhage.