右美沙芬在脑缺血中的神经保护作用  

Neuroprotection of dextromethorpham in rat middle cerebral artery occlusion model

作　　者：孙凤艳[1] 高骏[1] 张玲妹[1] 缪兵[1] 陆世铎[1] 程介士[1] 张安中[1] 

机构地区：[1]上海医科大学医学神经生物学国家重点实验室

出　　处：《中华神经外科杂志》1995年第S1期40-42,78-79,共5页Chinese Journal of Neurosurgery

基　　金：国家"八五"攻关课题

摘　　要：本文采用大鼠大脑中动脉阻塞致局灶性脑缺血模型，结合利用形态学、电生理学及分子生物学等多种实验方法，研究了右美沙芬在急性脑缺血再灌注后病理发展过程中的神经保护作用，以及其作用机制。实验结果揭示右美沙芬显著减少脑缺血致神经元死亡量，并呈时间依赖地加速脑缺血时及再灌注后大脑皮层体感诱发电活动的恢复作用。右美沙芬的神经保护作用机制之一可能与抑制脑缺血诱导的ＮＯＳｍＲＮＡ的表达作用有关。Abstract Middle cerebral artery occlusion model was used to induce cerebral ischemia in rats.Somatosensory evoked potential(SEP),HE staining and Northern Blot analysis were used to observe the neuroprotective effect and its mechanism of dextromethorpham in the pathological process during reperfussion followed by transient cerebral ischemia.The present results showed that dextromethorpham significantly decreases death neuron induced by ischemia and time-dependently improves the recovery of SEP during reperfusion after cerebral ischemia.The neuroprotection of dextromethorpham in this model probably relates to inhibit the over expression of NOS mRNA induced by cerebral ischemia.

关 键 词：右美沙芬 脑缺血 神经保护 一氧化氮合成酶 

分 类 号：R96[医药卫生—药理学]