血管性痴呆的动物模型及其胆碱能机制研究

目的 建立血管性痴呆（ＶＤ）的运行模型，并探讨血管性痴呆认知障碍的发病机制。方法 采用持久性双侧颈总动脉法致老龄大鼠慢必离血流灌注不足，建立老大鼠血管要模型，进行数字减影血管造影（ＤＳＡ）检查、穿梭箱试验和胆碱乙酰酶（Ｃｈｏｌｉｎｅ ａｃｅｔｙｉｔｒａｎｓｆｅｒａｓｅ，ＣｈＡＴ）免疫组化测定。结果 慢性脑血流灌注不足２月后出现明显的认知功能障碍，缺血４月后更明显；海马ＣＡ１区ＣｈＡＴ免疫反应阳性神

Establishment of a rat model of vascular dementia and study of its cholinergic mechanism

Objective To establish an animal model of vascular dementia(VD) in aging rat and study the mechanism of hypomnesis in vascular dementia. Methods An animal model of VD was established through chronic hypoperfusion of cerebral blood flow of the forebrain in aging rats with permanent bilateral common carotid arteries occlusion. The rats were tested with a computerized shuttle-training case. The changes of cerebrovascular system were observed with digital subtraction angiography(DSA). The brain tissues were studied for choline acetyltransferase(ChAT) with immunohistochemistry. Results The congnitive function of rats was obviously reduced after 2 months of the chronic erebral hypoperfusion and became worse after 4 months of hypoperfusion. The distribution and number of the neutrons positive to ChAT-like immunoreaction in the CA1 sector of the hippocampus were more significantly reduced in the hypoperfused rats than in those of the control and the decrease of the positive neutrons was positively correlated to memory disorders. Conclusion Our rat model of VD can reliably simulate the clinical manifestation of VD in human being resulting from chronic hypoperfusion of cerebral blood flow. Damages of cholinergic neurons in the cortex of the frontal lobe and hippocampus are the morphological basis of impairment of the cognition function.