【摘要】 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。更多还原

【Abstract】 Sixty four seven-day postnatal Wistar rats were divided randomly into 2 groups, hypoxic ischemic group and hypoxic ischemic plus SOD group. According to the duration of asphyxia,each group was subdivided into 4 small groups,the group of 30,60 and 120 minutes and acontrol group. The results showed that contents of LPO,GLU, ASP and water in brain tissue of hypoxic ischemic groups at different times after asphyxia were higher than those of thecontrol groups. The level of SOD was negatively correlated with the content of water inbrain tissue. There was notable difference in LPO,GLU,ASP and water contents of brain tissue between corresponding subgroups of the two big groups and the pathological changesconformed to it. These evidences indicate that OFR and EAA participate in the pathologicalprocess of hypoxic ischemic encephalopathy and that exogenous SOD can protect postnatalrats from brain damage caused by asphyxia.更多还原