蛛网膜下腔出血诱导小鼠长期认知功能损害

目的了解蛛网膜下腔出血（SAH）小鼠模型是否存在认知功能损害及探讨造成认知功能损害的可能机制。方法经枕大池注射自身动脉血建立SAH小鼠模型;14d时测量大脑主要动脉直径;通过8一臂迷宫实验评估SAH30d后动物空间学习和记忆功能;加高效液相色谱分析海码组织谷氨酸和天门冬氨酸水平。结果SAH后2周,大脑主要动脉无明显痉挛;SAH30d后,小鼠工作记忆能力和参考记忆能力明显低于对照组和假手术组（P〈0．05）;SAH后24h、48h和72h,海马区谷氨酸和天门冬氨酸含量明显增高（P〈0．01）,30d后,这两种氨基酸的浓度明显下降（P〈0．05）。结论SAH不引起迟发性脑血管痉挛,但可引起小鼠长时间认知功能损害。SAH引起急性脑血流量降低,海马区兴奋性氨基酸大量释放,可能引起海马区神经细胞损害,迟发性海马区兴奋性氨基酸（EAA）降低和认知功能损害是海马损害后的结果。

Induction of long-term cognitive dysfunction in mice after subarachnoid hemorrhage

Objective To investigate the long-term cognitive dysfunction of mice after subarachnoid hemonhage（SAH） and its possible mechanisms. Methods Murine models of SAH induced with blood injection into magna cysterna and major cerebral arteries were measured at 14 d after SAH. Spatial learning and memory ability was tested with 8-arm radial maze（8-ARM） at 30 d after surgery. The concentraton of glutamate and aspartate in hippocampus were tested with high performance liquid chromatography analysis. Results No significant spasm was found in SAH mice in main cerebral arteries at 14 d after SAH. Compared with control and sham mice, SAH mice showed significant lower correct rate in 8-ARM working memory task and reference task （P 〈 0.05） at 30 d after SAH. Increased concentrations of glutamate and aspartate in hippocampus were tested at 24 h,48 h and 72 h post-SAH（P 〈0.01 ） and decreased concentrations of glutamate and aspartate in hippocampus were tested 30-day post-SAH （P 〈 0.05） in SAH mice. Conclusions The study shows that long-term cognitive dysfunction occurs in SAH mice without delayed vasospasm, and SAH could induce early acute increasion in concentrations of exciting amino acids in hippocampus,which may cause hippocampal injury. Cognitive dysfunction and delayed decreasion in concentrations of exciting amino acids in hippocampus is the result of hippocampal injury.