摘要
目的 :通过检测不同时间局灶性脑缺血 /再灌损伤时活体脑片Ca2 + 的变化 ,希望揭示Ca2 + 在体水平脑缺血 /再灌损伤机制。方法 :用插线法制作局灶性脑缺血 /再灌损伤模型 ,激光扫描共聚焦显微镜观察活体脑片细胞内Ca2 + 的分布及动态变化。结果 :①随着缺血时间的延长 ,皮质及纹状体区域脑片细胞内Ca2 + 含量逐渐增加 ;②缺血 1h后再灌注 1 0min可引起脑片纹状体区域细胞内Ca2 + 含量明显增加 ,但将再灌时间延长至 3h ,Ca2 + 含量较灌注 1 0min为低 ;③缺血 6h皮质及纹状体区域脑片细胞内Ca2 + 含量明显多于缺血 1h ,再灌注 3h后 ,细胞内Ca2 + 含量有所下降 ,但仍高于假手术组 ;④纹状体对缺血 /再灌注损伤比皮质敏感。结论 :在脑缺血再灌注损伤中 ,皮质、纹状体部位的Ca2 +
AIM: The purpose of the present study was to detect intracellular Ca 2+ changes in living brain slices during focal cerebral ischemia/reperfusion (I/R) and reveal the role of intracellular Ca 2+ in the cerebral I/R injury. METHODS: The model of focal cerebral I/R was established in rats by reversible inserting a nylon thread, and dynamic change of intracellular Ca 2+ in brain slices was determined using laser confocal imaging system. RESULTS: ① Ca 2+ gradually enhanced with increase in ischemic time in cortex and striatum. ②At 1 h ischemia/ 10 min reperfusion, Ca 2+ increased significantly in striatum, but Ca 2+ decreased at 3 h reperfusion compared with 10 min reperfusion. ③ Ca 2+ markedly enhanced at 6 h ischemia compared with 1 h ischemia, and after 3 h reperfusion Ca 2+ decreased, but was still higher than that in sham-operation group. ④The striatum is more sensitive than cortex to ischemia/reperfusion. CONCLUSION: Ca 2+ overload in the area of cortex and striatum may play an important role in cerebral ischemia/reperfusion injury in rats.
出处
《中国病理生理杂志》
CAS
CSCD
北大核心
2002年第11期1357-1359,共3页
Chinese Journal of Pathophysiology
基金
"九五"国家医学科技攻关项目 (96 - 90 6 - 0 2 - 2 1 )