全脑缺血再灌注小鼠额叶、海马区神经元损伤的病理研究

Pathological research in neuron damage after repetitive ischemia-reperfusion of rat's frontal cortex and hippocampus histology

目的探讨全脑缺血再灌注小鼠中枢神经细胞损伤情况。方法采用重复阻断小鼠双侧颈总动脉并尾部放血(放血量小于体重的6%)再灌注的方式,建立了小鼠卒中模型。在此模型基础上,采用病理学技术,对脑缺血再灌注后小鼠额叶、海马区脑组织形态变化变化进行观察。结果重复缺血再灌注1 d神经细胞间质水肿,胞核浓染、固缩,再灌注3 d,额叶皮层少量胶质细胞增生;海马可见颗粒细胞呈空泡样变性。缺血再灌注7 d,皮层多量的小胶质细胞增生聚集成堆;海马CA1区锥体细胞变性,且部分坏死。缺血再灌注28 d,皮层神经细胞明显减少;海马CA1、CA3区锥体细胞大量缺失、变性、坏死,齿状回颗粒细胞变性呈空泡样。结论脑缺血再灌流中存在迟发性神经元死亡。

Objective To explore nerve central neuron damage of frontal cortex and hippocampus histology with repetitive ischemiareperfusion. Methods The stroke model rats were established by repetitively blocking bilateral common carotid arteries and exangulnating caudal vein （blood volume was less than 6%of body weight） and refilling. The changes in cerebral tissue configuration of front cortex and hippocampus of ischemia-reperfusion rats were observed by pathological technique. Resulls There were intercellular substance edema, stained nucleus and pyknosis 1 day after ischemia-reperfusion; there were a small quantity of hyperplastic glial cells in front cortex, and vacuolus degeneration in granular cells in hippocampus 3 days after ischemia-reperfusion; there were abundant hyperplastic glial cells in front cortex, pyramidal cell degeneration with partial necrosis in CA1 region ; there were obviously less neurons in cortex, pyramidal ceils absence, degeneration and necrosis in CA1 and CA2 region in hippocampus, and vaculous degeneration in granular cells in dentate gyms. Conclusions There are delayed neurons apoptosis in repetitive cerebral ischemia-reperfusion.