SOD与尼莫地平对窒息幼兔脑组织的保护作用  

Protective effect of SOD and nimodipine on cerebral injury of asphyxial young rabbit

作　　者：郝翼中[1] 刘立新[1] 王阿琚[1] 

机构地区：[1]山西医学院第一附属医院儿科

出　　处：《中国病理生理杂志》1994年第5期537-540,共4页Chinese Journal of Pathophysiology

摘　　要：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。young rabbits were divided into four different groups, which werecontrol,asphyxial, asphyxia treated with SOD,asphyxia treated with nimodipine. Bloodwere drawn from the heart of all animals 24 hours after the start of experiment.Theblood were tested for OFR,H_2O content of cerebral tissue and pathological changes ofcerebral tissue were also observed.We compared asphyxial with control group and foundthat in aspyxial group serum LPO and H_2O of cerebral tissue were increased markedly,while blood SOD and GSH-Px decreased significantly.Pathologic changes in the brainwere obvious and serum LPO was in a positive correlation with H_2O content of cerebraltissue. Compared two treated groups with asphyxial group,serum LPO and cerebral H_2Oof the treated groups decreased significantly, while SOD and GSH-Px increased significantly,and pathologic changes in brain were relieyed.It was concluded that OFR induced damagein brain subjected to acute asphyxia. Foreign SOD and nimodipine effectively prcventeddamage of the brain tissue of young rabbit.

关 键 词：窒息 脑损伤 氧自由基 钙通道阻滞剂 SOD 

分 类 号：R972[医药卫生—药品] R722.120.5[医药卫生—药学]