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目的:观察比较醒神解毒方预处理与缺血预处理减轻全脑缺血再灌注大鼠海马神经元损伤的作用。方法:实验选用24只雄性SD大鼠,随机将24只大鼠分为假手术组、缺血预处理组、药物处理组、脑缺血再灌注组,采用热凝椎动脉,钳夹双侧颈总动脉建立全脑缺血模型,缺血预处理组预缺血3min,3天后给予缺血10min,再灌注24h后处死。假手术组暴露双侧颈总动脉不夹闭。缺血再灌注组,夹闭双侧大脑颈总动脉10min,再灌注24h后处死。药物预处理组,灌胃2周后,做缺血再灌注处理,运用HE染色光镜下观察存活海马神经元细胞数,电镜下观察海马神经元超微形态的改变。结果:药物预处理存活神经元与缺血预处理存活神经元比较,P>0.05,两者与缺血再灌注比较,P<0.01。假手术组可见海马神经元细胞形态正常,脑缺血预处理组和药物预处理组海马CA1区神经元损伤明显减轻,只有少量细胞有轻度水肿,未见坏死。而脑缺血再灌注组神经元变性严重。结论:药物预处理对随后的脑梗死有明显的保护作用,能诱导缺血耐受的产生。
OBJECTIVE: To observe the effects of Xingshen Jiedu Fang preconditioning and ischemia preconditioning on neuronal damage in hippocampus during global cerebral ischemia-reperfusion in rats. Methods: Twenty-four male Sprague-Dawley rats were randomly divided into sham operation group, ischemic preconditioning group, drug treatment group, cerebral ischemia-reperfusion group, The model of global cerebral ischemia was established in the common carotid artery. The ischemic preconditioning group was ischemic preconditioned for 3 min and ischemia for 10 min after 3 days and then sacrificed 24 h after reperfusion. Sham operation group exposed bilateral common carotid artery is not closed. Ischemia-reperfusion group, occlusion of bilateral cerebral common carotid artery 10min, 24h after reperfusion were sacrificed. The rats in the drug pretreatment group were treated with ischemia / reperfusion 2 weeks after gavage. The number of surviving hippocampal neurons was observed under HE staining and the ultrastructure of hippocampal neurons was observed under electron microscope. Results: Compared with ischemic preconditioning surviving neurons, the survival neurons of pretreatment with P <0.05, P <0.01. The neurons in hippocampus were found to be normal in sham-operation group. Neuronal damage in hippocampal CA1 subregion was significantly alleviated in cerebral ischemic preconditioning group and drug pretreatment group. Only a few cells had mild edema and no necrosis. The neuronal degeneration in cerebral ischemia-reperfusion group was serious. Conclusion: The drug pretreatment has a significant protective effect on the subsequent cerebral infarction, can induce the generation of ischemic tolerance.