血管性痴呆大鼠脑血流量及细胞凋亡的研究

目的　研究脑血流量及细胞凋亡在血管性痴呆 (VD)发病机制中的作用。方法　采用双侧颈总动脉永久结扎方法制备前脑缺血致血管性痴呆动物模型 ,利用激光多普勒血流仪检测各组大鼠术后不同时间点 (术后 2 4h、1周、0 .5、1、2、3及 4个月 )额叶皮质、海马区局部脑血流量 (rCBF) ;采用HE染色、光镜观察各组大鼠脑组织的形态学变化 ;采用流式细胞仪 (FCM) ,观察额叶皮质、海马区神经细胞凋亡时程变化情况。结果　大鼠术后额叶皮质、海马区的rCBF明显下降 ,以术后 2 4h最明显 ,至术后 4个月时仍明显低于正常 ;病理学研究发现 ,少数大鼠出现脑梗死灶。随着脑血流量持续下降 ,额叶皮质经历了从锥体细胞水肿、缺血、凝固性坏死到变性、脱失及星形胶质细胞增生的过程 ;海马CA1区锥体细胞从最初的缺血、水肿逐渐发展为严重脱失、基质疏松及微空泡形成。FCM结果显示 ,额叶皮质及海马区细胞凋亡均在 1周时最明显 ,额叶皮质至术后 2个月、海马区至术后 3个月时仍明显高于对照组。海马区凋亡细胞百分率明显高于额叶皮质。结论　持续性脑血流量下降引起神经细胞凋亡是导致血管性痴呆的主要原因之一。

Study of cerebral blood flow and apoptosis in vascular dementia rats

Objective To study the roles of cerebral blood flow(CBF) and apoptosis in pathogenesis of vascular dementia(VD) of rats.Methods VD model was formed by adopting the permanent occlusion of bilateral common carotid arteries in Wistar rats to produce the forebrain ischemia.The laser Doppler was used to assess the cerebral blood flow.The neuropathological changes were observed with light microscope.The apoptosis was examined by the technique of flow cytometry(FCM).Results After the operation,the rCBF of the frontal lobe and hippocampus decreased obviously and progressively.There were infarction foci in a few rats.The diffused cerebral edema and exudation were apparent at the beginning,then attenuated gradually.The pyramidal neurons decreased progressively and microvacuolation was observed in hippocampus.FCM showed that the apoptosis in the ischemic group increased rapidly in the first week after operation,and lasted three months in frontal lobe,four months in hippocampus.Conclusion Apoptosis induced by cerebral hypoperfusion is one of the causes of VD.