脑缺血再灌注后海马CA1区谷氨酸的表达变化及氟桂利嗪的影响

目的　观察暂短性脑缺血再灌注后沙土鼠海马区谷氨酸的表达变化以及氟桂利嗪干预的影响。方法　按照Kirino的方法 ,制作缺血再灌注模型。于缺血再灌注后 1、2、7天采取免疫组化方法检测谷氨酸表达 ,并于 7天在电镜和光镜下观察组织学变化。结果　缺血再灌注组 1天及 2天海马CA1区谷氨酸表达增高 (P <0 .0 1) ,7天恢复正常。光镜及电镜可见给药组存活的神经元数目明显多于缺血再灌注组 (P <0 .0 1)。结论　谷氨酸表达增高可能是鼠脑海马区迟发性神经元死亡的原因之一 ,氟桂利嗪可抑制谷氨酸的表达 ,对缺血的神经元起保护作用。

Changes of glutamate expression in the CA1 region of hippocampus of gerbil brain following cerebral ischemia reperfusion and flunarizine's effect

Objective The effect of ischemia reperfusion on the expression of glutamate in the CA 1 region of hippocampus of gerbil brain was observed and flunarzine was used for studying whether it regulate the expression of glutamate under the condition of cerebral ischemia.Methods A transient ischemia and reperfusion model was established in rat according to kirino method. The expression of glutamate was examined at the 1st? 2nd and 7th day respectively. Macro and microscopical changes were observed at the 7th day after transient ischemia.Results The expression of glutamate increased at the 1st and 2nd day, returned to control's leveal at the 7th day after transient ischemia in the CA 1 region of ischemia group. Macro and microscopical changes in CA 1 region were less extensive in drag treated group than those in ischemia group at the 7th day after transient ischemia.Conclusions Up regulation of glutamate expression after transient ischemia may be one of the causes of the delayed neuronal death. Flunarizine could decrease the expression of glutamate and prevent the neurons from ischemia injury.