论文部分内容阅读
目的 探讨缺血预处理脑保护效应,以及神经细胞凋亡与缺血性脑损害的关系。方法 家兔15只,随机分为3 组,对照组(A组,n= 5),缺血组(B组,n= 5),缺血预处理组(C组,n= 5)。A组只做手术操作,B组采用二血管夹闭(双侧颈总动脉夹闭,MAP< 40m m Hg)全脑缺血10 分钟,C组在缺血前增加缺血预处理2分钟再灌注30 分钟。对比观察缺血后3 天海马CA1 区神经元密度和缺血细胞数,同时使用TUNEL原位标记法,检测缺血3天后海马区的凋亡细胞。结果 (1)C组神经元密度与A 组相比差异无显著性,与B组相比神经元密度显著增加(P< 0.05);(2)C组缺血细胞数较B组显著降低(P< 0.01),与A组相比差异无显著性,缺血预处理对海马CAl区内、中、外段分别起到88% 、84% 、76% 的保护作用;(3)TUNEL法显示B组短暂脑缺血后迟发性神经元死亡中发现神经细胞凋亡,而A组未发现。结论 (1)缺血预处理后30 分钟确能对再次缺血发挥脑保护作用;(2)脑缺血可能促进神经细胞凋亡。
Objective To investigate the protective effect of ischemic preconditioning on cerebral ischemia and the relationship between neuronal apoptosis and ischemic brain damage. Methods Fifteen rabbits were randomly divided into 3 groups: control group (group A, n = 5), ischemic group (group B, n = 5) and ischemic preconditioning group (group C, n = 5). Group A was operated only in two groups. Group B received occlusion of the common carotid artery (bilateral common carotid artery occlusion, MAP <40 m Hg) for 10 min after ischemia. Group C received ischemic preconditioning for 2 min before ischemia Perfusion for 30 minutes. The neuronal density and number of ischemic cells in hippocampal CA1 area were observed and compared 3 days after ischemia, and apoptotic cells in hippocampus were detected by TUNEL in situ 3 days after ischemia. Results (1) There was no significant difference in density of neurons between group C and group A (P <0.05). (2) Compared with group B, the number of neurons in group C was significantly higher than that of group B (P <0.01). Compared with group A, there was no significant difference in ischemic preconditioning, and ischemic preconditioning could protect 88%, 84% and 76% ) TUNEL method showed that neuronal apoptosis was found in the delayed neuronal death in group B after transient ischemic attack, but not in group A. Conclusion (1) Ischemia preconditioning can exert cerebral protective effect on ischemic preconditioning for 30 minutes. (2) Cerebral ischemia may promote neuronal apoptosis.