大鼠脑缺血再灌流期海马内缩胆囊素的动态变化  

Dynamic Changes of Cholecystokinin After Brain Ischemia and Recirculation in Rat Hippocampus

作　　者：刘兴材[1] 孙卫文[2] 许海雄[1] 吴莹[1] 陈玲[1] 龚素珍[2] 金钦华[1] 

机构地区：[1]汕头大学医学院第二附属医院神经内科 [2]广州医学院神经科学研究所

出　　处：《广州医学院学报》1998年第1期6-9,共4页Academic Journal of Guangzhou Medical College

摘　　要：本实验采用免疫组化技术，研究了脑缺血及再灌流各阶段大鼠海马内缩胆囊素（CCK）的变化，再灌流后6～24h，海马CCK阳性神经元有所增多，再灌1天后CCK阳性细胞有所减少，至第4～7天时CCK阳性神经元减少更明显，脑缺血性改变于再灌流6h以前呈现加重趋势，1天后乃逐渐改善，至第4～7天时CA2～4区的缺血变化显著减轻，而在CA1区，随着再灌流期延长，其缺血性变化不仅不改善，反而加重直至部分锥体细胞死亡。提示：CCK的大量释放可能与脑缺血再灌流神经损害有关。The aim of this article is to study the change of cholecystokinin(CCK) during recirculation (Rec. ) after brain ischemia. Immunohistochemical staining for CCK and Nissl staining was used to study all l2 groups. We found immunopositive CCK (+ ) neurones and products in all hippocampal areas (CA,CA4) increased noticiably during Rec. 6h-12h, but decreased after Rec.1d. CCK (+ ) neurons further decreased on Rec. 4d-7d. The decreased of CCK (+ ) neurons might be attributed to the release of quite an amount of CCK and also due to the actual loss CCK neurons. The ischemic changes advanced before Res. 6h and gradually improved after Red. 1d.We found that ischemic changes much improved in hippocampal areas CA-CA4 but aggravated in CA, during Rec. 4d-7d. Our results suggest that the release of CCK may play some role in the development of cerebral ischemia/recirculation neuronal damage.

关 键 词：脑缺血 再灌流 海马 缩胆囊素 

分 类 号：R364[医药卫生—病理学]