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目的 :通过对大鼠局灶性脑缺血再灌注海马 CA1区神经元形态学观察 ,探讨高血糖对海马迟发性神经元死亡的影响。方法 :术前给大鼠腹腔内注射生理盐水和葡萄糖造成正常血糖和高血糖状态 ,参考 Zea- L onga法制备大脑中动脉阻塞及再灌注模型。于再灌注后 1、3、7d取材 ,进行 HE染色 ,观察正常神经元。结果 :缺血再灌注后 1、3、7d正常血糖组海马 CA1区正常神经元计数为 1 76.0 0± 4.2 4 ,1 1 0 .75± 7.89,5 9.0 0± 8.41 ;高血糖组为1 68.2 5± 7.1 4,89.5 0± 8.2 0 ,39.75± 8.42 ,3d和 7d时两组之间存在显著性差异 ( P<0 .0 5 )。结论 :高血糖可加重局灶性脑缺血再灌注后海马 CA1区迟发性神经元死亡
OBJECTIVE: To investigate the effects of hyperglycemia on the neuronal death in the hippocampus of rats after focal cerebral ischemia reperfusion. Methods: Normal rats were given intraperitoneal injection of normal saline and glucose to induce normal blood glucose and hyperglycemia. Zea L onga method was used to prepare middle cerebral artery occlusion and reperfusion models. At 1, 3, 7 days after reperfusion, HE staining was performed to observe normal neurons. Results: The normal neurons in hippocampal CA1 area of normal blood glucose group at 1, 3, 7 days after ischemia / reperfusion were 1 76.0 0 ± 4.2 4,1 10.7 ± 7.89 and 5 9.0 0 ± 8.41, respectively. The hyperglycemia group was 1 68.2 5 ± 7.1 4,89.5 0 ± 8.2 0, 39.75 ± 8.42, 3d and 7d there was a significant difference between the two groups (P <0.05). Conclusion: Hyperglycemia can aggravate delayed neuronal death in CA1 area of hippocampus after focal cerebral ischemia-reperfusion