【摘要】 目的探讨老年脑缺血/再灌注(I/R)脑微血管生成的意义。方法SD雄性青年和老龄大鼠,随机分为青年假手术组、青年模型组、老龄假手术组、老龄模型组;模型组分为脑缺血3h、I/R1d、3d、6d、12d时间点。采用线栓法制备局灶性脑I/R模型,测定脑微血管密度(MVD)、血管场面积、神经细胞凋亡数以及脑组织病理改变等。结果老龄模型组I/R6d、12d MVD较老龄假手术组降低(P<0.05,P<0.01),I/R 1d血管场面积较老龄假手术组增高(P<0.05);与青年组同时间点分别比较,老龄假手术组MVD增高(P<0.01),老龄模型组I/R 1d、3d、6d、12d大鼠MVD、血管场面积均降低(P<0.05,P<0.01)。老龄模型组MVD自脑缺血3h持续下降至I/R 12d;血管场面积于I/R 1d达峰值,后逐步下降。老龄模型组I/R 1d、3d、6d、12d大鼠神经细胞凋亡数较其假手术组增多(P<0.05,P<0.01);与青年组同时间点分别比较,老龄假手术组及模型组I/R3d、6d神经细胞凋亡数增多(P<0.01)。老龄模型组神经细胞凋亡数I/R 3d达峰值,I/R 3~12d逐渐减少。脑组织病理改变方面,老龄模型组脑缺血3h开始出现病理变化,I/R 1d逐渐加重,I/R 3d损伤达到高峰,I/R 6~12d损伤逐渐减轻;此变化过程中老龄模型组较青年模型组损伤严重。结论老年脑缺血/再灌注脑组织损伤严重并提前出现,神经细胞凋亡显著且发生的时间早,微血管损伤明显且再生减弱,这些变化可能与增龄有关。更多还原

【Abstract】 Objective To study the significance of cerebral angiogenesis after cerebral ischemia/reperfusion in aged rats.Methods Young and aged masculine SD rats were randomly divided into sham operated group and model group.Model group were subjected to 3h of middle cerebral artery occulsion with the intraluminal filament technique,then followed by reperfusion of 1d,3d,6d and 12d.The microvessel density(MVD) of brain tissue,sum area of lumens,apoptosis counts of nerve cells and brain cell ultrastructure were examined.Results Compared with aged sham operated group,MVD in that model group at I/R 6d and 12d were decreased(P<0.05,P<0.01),sum area of lumens in that model group at I/R 1d was increased(P<0.01).Compared with young group at the same time points,MVD in aged sham operated group were increased(P<0.01),MVD and sum area of lumens in aged model group at I/R 1d,3d,6d and 12d were decreased(P<0.01).MVD in aged model group lasted to descend from I 3h to I/R 12d.Sum area of lumens in aged model group reached peak at I/R 1d,gradually decreased subsequently.Compared with sham operated group,apoptosis counts of nerve cells in aged model group at I/R 1d,3d,6d and 12d were increased(P<0.05,P<0.01).Compared with young group,apoptosis counts of nerve cells in aged sham operated group and that model group at I/R 3d,6d were increased(P<0.01).Apoptosis counts of aged model group reached peak at I/R 3d,decreased gradually at I/R 3d~12d.In aspect of brain cell ultrastructure,the starting occurrence of pathological change in aged model groups appeared at I 3h,aggravated gradually,and then reached the injury peak at I/R 3d,became alleviated gradually at I/R 6d~12d.In this varied process,aged model suffered more serious damages than young model.Conclusions The mechanisms of the changes that severe cerebral injury appeared in advance,striking apoptosis of nerve cells occurred early,obviously damaged cerebral micrangium as well as weakly regeneration after cerebral ischemia/reperfusion in the aged might be closely related to aging.更多还原