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64只新生Wistar大鼠，随机分成缺氧缺血组和缺氧缺血＋SOD组两大组；两大组又再分为对照组、窒息后30min、60min和120min4小组。结果：缺氧缺血组中对照组与窒息后各不同时间组比较，脑组织中过氧化脂质（LipidperoxideLPO）、谷氨酸（GLu）、天门冬氨酸（ASP）及脑水含量明显升高；组织SOD与脑水含量呈负相关关系；两大组间各相应时间组中LPO、GLu、ASP和脑水一有明显差异，且病理改变与之相符。提示氧自由基（OFR）与兴奋性氨基酸（EAA）共同参与了缺氧缺因性脑病的病理过程；外源性SOD对窒息幼鼠所致的缺氧缺血性脑病具有保护作用。且得到病理检查支持。
Sixty-four fresh Wistar rats were randomly divided into two groups: hypoxic-ischemic group and hypoxic-ischemic + SOD group. The two groups were divided into control group, 30 min, 60 min and 120 min after asphyxia group. Results: Compared with different time groups, the contents of lipid peroxidation lipoprotein (LPP), glutamate (GLu), aspartate (ASP) and brain water in control group and hypoxia-ischemia group were significantly increased High; tissue SOD and brain water content was negatively correlated; LPO, GLu, ASP and brain water in the corresponding time between the two groups were significantly different, and the pathological changes in line with them. It is suggested that OFR and EAA participate in the pathogenesis of hypoxic-deficient encephalopathy. Exogenous SOD may protect hypoxic-ischemic encephalopathy induced by asphyxia in rats. And get pathological examination support.