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４２只新西兰幼兔，随机分为对照、窒息、窒息＋ＳＯＤ及窒息＋尼莫地平４组。各组动物均于实验开始后２４ｈ心脏取血测ＯＦＲ，测脑组织水含量，并观察脑病理改变。窒息组织与对照组比较，血清ＬＰＯ、脑水含量明显增高，血中ＳＯＤ，ＧＳＨ－Ｐｘ活力明显降低，脑病理改变明显，且窒息组ＬＰＯ与脑水含量呈正相关关系。两用药组与窒息组相比，血清ＬＰＯ、脑水含量明显减少，ＳＯＤ、ＧＳＨ－Ｐｘ活力明显增高，脑病理改变减轻。提示ＯＦＲ参与了窒息所致脑损伤的病理过程，外源性ＳＯＤ和尼莫地平对窒息幼兔脑组织有保护作用。
Forty-two New Zealand rabbits were randomly divided into 4 groups: control, apnea, asphyxia + SOD and asphyxia + nimodipine. Each group of animals at the beginning of the experiment 24h after heart blood OFR, measuring the water content of brain tissue, and observe the pathological changes of the brain. Compared with the control group, the levels of serum LPO and brain water in asphyxiated group were significantly increased, the activities of SOD and GSH-Px in blood were significantly decreased, and the pathological changes were obvious. The LPO and the water content in asphyxia group were positively correlated. Compared with asphyxia group, the serum LPO and brain water content decreased significantly, the activity of SOD and GSH-Px increased significantly and the pathological changes of brain decreased. The results suggest that OFR is involved in the pathological process of asphyxial brain injury. Exogenous SOD and nimodipine have protective effects on asphyxiated young rabbits.