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目的 :研究沙土鼠短暂性脑缺血后海马 CA 1区细胞凋亡及亚低温的治疗作用。方法 :阻断沙土鼠双侧颈总动脉 2 0分钟造成前脑缺血模型。实验动物被随机分为假手术组、缺血再灌注组、亚低温治疗组。海马CA1区的迟发性神经元死亡 (DND)过程通过序列光镜观察进行研究 ,原位末端标记 (TU NEL)法用来检测死亡神经元的 DNA片断。结果 :短暂性脑缺血后 ,海马 CA1区锥体神经元于再灌注后 2～ 7日死亡。死亡锥体神经元的序列光镜观察没有发现早期的凋亡样改变 ,DNA片断化也发生在 DND出现之后。亚低温处理动物再灌注后 2～ 7日 ,海马 CA 1区缺血性神经元死亡较常温处理动物显著减轻 ,再灌注后 3～ 7日 ,海马 CA 1区 DNA片断化也显著减少。结论 :缺血后的亚低温治疗产生了神经保护作用 ,而抑制神经元 DNA片断化的出现可能是其保护机制之一。
Objective: To study the therapeutic effect of hypothermia on apoptosis and hippocampal CA 1 area after gerbil transient cerebral ischemia. Methods: Blocking bilateral common carotid arteries in gerbils caused forebrain ischemia at 20 minutes. The experimental animals were randomly divided into sham operation group, ischemia-reperfusion group and mild hypothermia treatment group. The delayed neuronal death (DND) process in the hippocampal CA1 region was studied by sequential light microscopy. The TU NEL method was used to detect DNA fragments of the deceased neurons. Results: After transient cerebral ischemia, pyramidal neurons in CA1 area of hippocampus died 2 ~ 7 days after reperfusion. The apoptotic pyramidal neurons showed no early apoptosis-like changes observed by light microscopy. DNA fragmentation also occurred after the appearance of DND. The hypoxic ischemic neuronal death in CA 1 area of hippocampus was significantly reduced from 2 to 7 days after mild hypothermia in animals treated with normal temperature. The DNA fragmentation in CA 1 area of hippocampus was also significantly reduced from 3 to 7 days after reperfusion. CONCLUSION: Mild hypothermia after ischemia produces neuroprotective effects, and inhibition of neuronal DNA fragmentation may be one of its protective mechanisms.