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目的探讨血管壁炎症反应和细胞凋亡在CVS发病机制中的作用。方法枕大池二次注血法建立大鼠SAH后CVS模型,60只大鼠分为SAH组及对照组,每组按建模后1d、3d、7d、11d、14d分为5个亚组,分别测量基底动脉直径、基底动脉ICAM-1的OD值及凋亡指数。结果 SAH后第1天血管壁ICAM-1升高,第3天达高峰,第7天后逐渐下降,第11天正常;SAH后第1天在血管壁凋亡细胞增多,第7天达高峰,第14天仍高于对照组。结论血管壁的炎症反应及细胞凋亡在SAH后CVS中均发挥着重要作用,其起始及进展过程还需要进一步的深入研究。
Objective To investigate the role of vascular wall inflammation and apoptosis in the pathogenesis of CVS. Methods CVS model of rats after SAH was established by the secondary injection of occipital cistern and 60 rats were divided into SAH group and control group. Each group was divided into 5 subgroups at 1d, 3d, 7d, 11d and 14d after modeling, Baseline artery diameter, ICAM-1 OD value and apoptosis index were measured. Results The level of ICAM-1 in vessel wall increased on the first day after SAH, peaked on the third day, decreased gradually on the seventh day and normal on the eleventh day. After the SAH, the number of apoptotic cells increased on the first day and peaked on the seventh day, Day 14 is still higher than the control group. Conclusion The inflammatory reaction and apoptosis in the vascular wall play an important role in CVS after SAH. The initiation and progression of the disease still need further study.