摘要
在大鼠中用热凝造成大脑中动脉阻塞而致脑局灶性缺血。电镜观察发现,在缺血2min后,神经细胞粗面内质网与线粒体即出现改变。光镜检查,缺氧10min后才出现神经细胞缺血改变;梗死灶周边微血管体积密度在缺血24h后即明显升高。肉眼检查,于缺血3h后可见梗死灶。在缺血2min后,脑组织内丙二醛(MOA)即升高,说明在缺血缺氧的早期,脂质过氧化作用加强。表明自由基在缺血性脑损伤早期即起重要作用。
This paper reports the pathological changes and MDA content of the brain tissue in the early stage of cerebral ischemia due to middle cerebral artery occlusion (MCAO) in Wistar rats. The neurones showed changes of the rough endopiasmic reticulum and the mitochondrium as early as 2 minutes after MCAO. Under the light microscope, 'ischemsc cells' with shrunken and condensed cytoplasm and nucleus appeared 10 minutes after MCAO. The end-product of lipid peroxidation, MDA, in the isch. emic brain tissue also significantly increased 2 minutes after MCAO, being correlated synchronously with the ultrastructural changes of the neurones. This suggested that free radicals play a role in the early stage of brain injury due to ischemia.
出处
《中国病理生理杂志》
CAS
CSCD
北大核心
1991年第5期546-548,共3页
Chinese Journal of Pathophysiology
关键词
脑缺血
丙二醛
大鼠
Brain ischemia
Malondialdehyde
Rats