摘要
目的了解脑血管生成是否参与脑白质区域慢性低灌注状态下血脑屏障的破坏机制。方法将72只雄性Wistar大鼠随机分为3组:假手术组、脑缺血组、干预组,脑缺血组及干预组大鼠结扎双侧颈总动脉构建慢性低灌注模型,干预组给予血管生成抑制剂灌胃以抑制血管生成;对各组大鼠在相同时间点检测脑深部白质区域微血管密度、白质纤维密度以及伊文思蓝静脉注射6 h后脑白质区域组织内伊文思蓝水平。结果脑缺血组及干预组大鼠脑白质区域血管密度和伊文思蓝浓度均显著高于假手术组,白质纤维密度显著低于假手术组,干预组微血管密度、白质纤维密度及脑组织内伊文思蓝水平显著低于脑缺血组。结论慢性低灌注诱导的血管生成可能导致血脑屏障通透性增加,但血管生成有助于减轻白质损伤,但这种保护作用大于血脑屏障通透性改变带来的不利影响。
Objective To estimate the influence of angiogenesis on blood-brain barrier damage mechanism under chronic cerebral hypoperfusion status of white matter.Methods Seventy-two male Wistar rats（250-350 g） were divided into three groups： sham-control group, ischemia group and anti-angiogenesis group. Permanent and bilateral common carotid artery occlusion was used to induce hypoperfusion of forebrain in the ischemia group and anti-angiogenesis group, and oral gavage with souvenir was used for anti-angiogenesis administration. Capillary density, Kluver-Barrera＆#39;s myelin sheath staining and quantitative measurement of Evans Blue were made at the 30th day after the operation.Results Compare to the sham-control group, the ischemia group and anti-angiogenesis group had higher capillary density, higher concentration of Evans Blue and lower density of white matter fibers. The capillary density, the concentration of Evans Blue and the density of white matter fibers in the anti-angiogenesis group were much lower than those in the ischemia group.Conclusion The angiogenesis induced by chronic cerebral hypoperfusion states could lead to blood-brain barrier disruption. However, the protective effect of angiogenesis on white matter overwhelmed the bypass adverse effect of subsequent blood-brain barrier disruption.
出处
《卒中与神经疾病》
2017年第3期181-184,共4页
Stroke and Nervous Diseases
关键词
脑缺血
血脑屏障
血管生成
白质损害
Brain ischemia
Blood-brain barrier
Angiogenesis
White matter impairment
