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夹闭沙土鼠双侧颈总动脉30min后恢复血流制作脑缺血再灌流模型。采用透射电镜观察额叶皮质超微结构。表明在神经元发生进行性破坏改变的同时,伴随着神经胶质细胞反应性增加、肥大、水肿、变性、坏死和解体等一系列改变。启示其可能参与神经元在缺血条件下代谢的调整。其后神经胶质细胞本身的退行性改变促进了神经元的不可逆性损伤。毛细血管壁的损伤和血管周围水肿可能是引起再灌流障碍的主要原因之一。
After occluding bilateral common carotid arteries of gerbils for 30 minutes, the blood flow was recovered and the model of cerebral ischemia-reperfusion was established. Transmission electron microscopy was used to observe the ultrastructure of frontal cortex. It shows that in the process of progressive destruction of neurons, glial cell reactivity is accompanied by a series of changes such as hypertrophy, edema, degeneration, necrosis and disintegration. It is suggested that it may be involved in the regulation of neuronal metabolism under ischemic conditions. Subsequent degenerative changes of glial cells promote the irreversible damage of neurons. Damage to the capillary wall and perivascular edema may be one of the major causes of dysfunction of reperfusion.