摘要
目的通过对蛛网膜下腔血性、非血性刺激物对脑血管影响的比较,探讨蛛网膜下腔出血(SAH)后迟发性脑血管痉挛(DCVS)的发病机制。方法将40只新西兰白兔随机分为5组:假手术组、非抗凝自体动脉血组、抗凝自体动脉血组、Kaoline(高岭土)组和失活细菌组,每组8只。假手术组动物仅做枕大池假穿刺;非抗凝血组动物采用经枕大池二次注血法制作DCVS模型;抗凝自体动脉血组用肝素处理后的自体动脉血代替非抗凝血行枕大池二次注血;Kaoline组和失活细菌组经枕大池穿刺分别注入15%Kaoline悬浊液(0.25ml/kg)、失活细菌悬浊液(3×1010个/ml;0.25ml/kg)。各组受试动物在7d时用4%多聚甲醛灌注处死,将脑组织连同基底动脉及其分支取出行HE染色、免疫组化检测TNF-α供组织学研究。结果与假手术组基底动脉血管形态相比,非抗凝血组、Kaoline组和失活细菌组均有不同程度的血管痉挛,抗凝血组无明显血管痉挛。TNF-α表达随血管痉挛程度加重而增加。结论蛛网膜下腔内不同刺激物导致与SAH后DCVS相同的病理改变提示:蛛网膜下腔内刺激物所致血管局部的过度炎症反应可能是导致血管痉挛发生的重要原因。
Objective To investigate mechanism about delayed cerebral vasospasm(DCVS) following subarachnoid hemorrhage(SAH) by comparing of histological varies of cerebral arteries which induced by injecting hematodes and non-hematodes stimulus into subarachnoid space.Methods 40 New Zealand white rabbits were divided into 5 groups randomly(n=8).Shamed-injection was completed only in Shamed-operation Group,DCVS model were made with two-hemorrhage of SAH by injecting autologous arterial blood into the cisterna magna of ...
出处
《脑与神经疾病杂志》
2011年第3期213-216,共4页
Journal of Brain and Nervous Diseases