光化学诱导鼠大脑中动脉闭塞及再通模型  

MCA thrombosis induced by photochemistry in rats: an experiment study

作　　者：王伟[1] 董为伟[1] 傅雅各 董强[1] 

机构地区：[1]同济医科大学基础医学院脑研究室,重庆医科大学神经病学研究所,上海医科大学华山医院神内科

出　　处：《中国神经精神疾病杂志》1996年第1期27-30,共4页Chinese Journal of Nervous and Mental Diseases

基　　金：国家自然基金

摘　　要：应用光化冷光源仪（金属卤化物灯）诱导鼠大脑中动脉（ＭＣＡ）闭塞，并于光照血管局部滴注尼莫地平致闭塞血管再通。结果发现：光照３０ｍｉｎ后鼠脑皮质及基底节局部脑组织血流量（ｒＣＢＦ）明显下降，且维持９０ｍｉｎ以上。同时，光照侧脑组织含水量明显增加。尼莫地平局部滴注２０ｍｉｎ后皮质ｒＣＢＦ则有所回升，用药后３０ｍｉｎｒＣＢＦ明显上升，为缺血前ｒＣＢＦ的１３１．１％。组织病理形态观察显示：光照例鼠ＭＣＡ及其周围毛细血管管腔内均有明显血栓形成，缺血１２ｈ梗塞区神经元、线粒体及内质同明显肿胀，神经元坏死。再灌注后病理损害更为明显。实验鼠先照例额、顶叶皮质及新纹状体出现边界清晰、范围较恒定的苍白梗塞灶。该模型的建立为进一步研究脑缺血及脑梗塞提供了新的工具。MCA occlusion was carried out photochemically by a halogenate light(a green, cool beam operating at a wave ength of 560um). At 60min after the induction of MCA thrombosis, 150ul of 20uM nimodipine was appled to the surface of MCA irradiated. It was found that 30min after irradiated,the rCBF of cortex and basal ganglia of irradiatedside decreased markedly by 71.3% and 59.5% respectively, and sustained for more than 90min. The brain water content of ischemia side more significantly increased than the control group (P<0.01). At 30min after nimodipine was topically appled, the rCBF of cortex dramatically increased to 131.1% by the level of before ischedria. All of rats irradiatedhad identigifiable areas of infarction in cortex and basal ganglia. After 6h ischemia, the results of histopathological showed that there were thrombus within MCA and capillary, and mild astrocytic swelling and neuronal necrosis on the cerebral cortex irradiated. However, severe stluctfal abnormalities were detected following recanalization.Inaddition, during 24h ischemia variable neurologic deficits were found in all rat irradiated.

关 键 词：脑梗塞 大脑中动脉 动物模型 光化学诱导 大鼠 

分 类 号：R743.33[医药卫生—神经病学与精神病学]