血管内皮细胞凋亡在兔脑血管痉挛模型的初步研究

发布时间：2018-05-17 09:30

  本文选题：脑血管痉挛 + 兔　； 参考：《苏州大学》2006年硕士论文

【摘要】： 本课题分两部分,第一部分主要研究兔血管内穿刺脑血管痉挛(Cerebral Vasospasm, CVS)模型的病理学变化;第二部分探讨血管内皮细胞凋亡在CVS痉挛血管中的表达。 第一部份兔血管内穿刺CVS模型的脑血管病理改变 目的:研究兔血管内穿刺模型的脑血管痉挛时间窗和脑血管形态学变化。 材料与方法:健康清洁级新西兰大白兔72只采用血管内穿刺法即经股动脉穿刺将导管插到兔颈内动脉,以导丝刺破颈内动脉,产生蛛网膜下腔出血(Subarachnoid Hemorrhage, SAH),制作CVS模型。存活兔子随机分成12小时、1天、2天、3天及7天组,共5大组。每组又根据导丝是否刺破颈内动脉分为SAH组(5只)及对照组(2只)。每只兔子术前、术后常规行头颅CT检查,SAH评估参考Fisher分级,分0-Ⅲ级。每只兔子处死后常规行HE染色观察后交通动脉及基底动脉管腔内直径及管壁厚度改变。选取12只兔子(对照组2只,每SAH组各2只)的右颈内动脉行透射电镜(Transmission Electron Microscope, TEM)观察血管壁超微结构改变。 结果:对照组10只及SAH组25只兔子获取脑组织标本。SAH组中,SAHⅠ级8只,Ⅱ级14只,Ⅲ级3只。同对照组相比,后交通动脉及基底动脉管腔内直径在SAH后12小时分别缩小了43.6%和51.82%。随后在1天～7天动脉呈持续性狭窄,管腔直径在第7天再次明显缩小,分别下降了29.32%和45.19%。7天组后交通动脉和基底动脉管壁厚度均明显增厚,分别增加了56.95%和44.33%。 结论:兔血管内穿刺CVS模型呈急性期收缩和迟发性收缩双相改变。其痉挛时间窗与血管形态学改变同人脑血管痉挛基本相仿。兔血管内穿刺CVS模型是研究人脑血管痉挛发病机制及治疗方法的适合模型。
[Abstract]:This study was divided into two parts. The first part was to study the pathological changes of Cerebral Vasospasm (CVS) model, and the second part was to investigate the expression of vascular endothelial cell apoptosis in CVS vasospasm. The first part of the CVS model of intravascular puncture in rabbits Objective: to study the changes of cerebral vasospasm time window and cerebral vascular morphology in rabbit intravascular puncture model. Materials and methods: 72 healthy and clean grade New Zealand white rabbits were inserted into the internal carotid artery by femoral artery puncture, and the subarachnoid hemorrhage (SAHN) was produced by the guide wire to puncture the internal carotid artery. The model of CVS was made by using subarachnoid hemorrhage (SAHX). Surviving rabbits were randomly divided into 5 groups: 12 hours, 1 day, 2 days, 3 days and 7 days. Each group was divided into SAH group (n = 5) and control group (n = 2). Before and after operation, each rabbit underwent routine head CT examination to evaluate the Fisher grade, which was divided into 0-鈪，

本文编号：1900850