实验性脑缺血组织自由基水平、神经病理与甘露醇作用机制的研究  

The study to experiment rabbit's cerebral ischemia their free radical neuropathology and the mechanism of mannital

作　　者：李长宏[1] 马文富[1] 田玲玲 

机构地区：[1]中国人民解放军第463医院神经内科

出　　处：《脑与神经疾病杂志》1996年第4期193-195,共3页Journal of Brain and Nervous Diseases

摘　　要：以家兔急性不完全性脑缺血模型，采用“电子自旋共振波谱（ＥｌｅｃｔｒｏｎＳｏｉｎＲｅｓｏｎｃｅ，ＥＳＲ）技术及电子显微镜，对实验性脑缺血组织自由基水平及神经病理进行研究，同时对甘露醇的作用机制进行探讨。结果证实，脑缺血后自由基水平明显增高，神经细胞、星形胶质细胞超微结构发生明显病理改变。而经甘露醇治疗后，自由基水平显著下降，与模型组比较，Ｐ＜０．０１，且大脑皮层细胞损伤程度较模型组明显减轻。这种抑制急性脑组织损伤的作用与甘露醇清除自由基功能及高渗作用密切相关。Abstract Eletron Soin Resonance (ESR),electron microscopy were used for rabbit's cerebral ischemic, to study the influenece of free radical and neuropathology and inquire to the mechanism of mannital function. Rasults showed that the level of radical has a marked increase and pathological change after cerebral ischemia. That the level of free radical had a decline and marked alleviation to cell of cerebral cortex compared with the group of model after the treatment was used by mannital (P<0.01).The action suppressing acute cerebral injure is closely related with the mannitol function scavening free radical and the hyperosmolar action.

关 键 词：脑缺血 自由基 神经病理 甘露醇 

分 类 号：R743.31[医药卫生—神经病学与精神病学] R983.1[医药卫生—临床医学]