减压后脑体积肿大的病理生理基础  

The Pathophysiological Basis of Brain Bulk Enlargement Following Decompression

作　　者：许百男[1] 段国升[1] 张纪[1] 

机构地区：[1]军医进修学院神经外科

出　　处：《军医进修学院学报》1993年第1期6-8,共3页Academic Journal of Pla Postgraduate Medical School

摘　　要：36只家猫按脑缺血(EEG平坦),(CBF为0)时间(25分钟、15分钟、5分钟)分为三组。每组均为12只,其中6只减压后注入2％Evans蓝(4mg/kg),另6只用于组织学检查。Evans蓝染色:急性脑肿大脑干及下血脑重度着色,而迟发性脑肿大大脑半球重度着色。组织学改变:急性脑肿大以脑干和下丘脑损伤、血管充血性扩张为主要改变、迟发性脑肿大以大脑半球水肿为主要改变。结论、脑干和下丘脑损伤而致脑血管麻痹性扩张,脑血容量增多即脑肿胀是急性脑肿大的主要病理生理基础。而缺血性脑水肿是迟发性脑肿大的主要病理生理基础。The purpose of this study was to further determine pathophysiological hasis of postdecompressive brain bulk enlargement(BBE)through the experiment of brain compression. 36 cats were divided into 3 groups according to the duration of global ischemia (flat EEG and no CBF), i, e. acute BBE with 25 minutes of ischemia, delayed BBE with 15 minutes of ischimia and no BBE with 5 minutes of ischemia 12 cats were included in each group. 6 cats were sacrificed in the end of experiment for histological examination, and other 6 cats were injected with 2% Evans blue (4 mg/Kg) and sacrificed at one hour later (3 cats) and the end of experiment (3 cats) respectively. Histologically, the vascular damage, dilation, bleeding and neuronal necrosis were found prominently in brain stem and hypothalamus in acute BBE. CereBral ischemic edema was observed mainly in gray and white matter of cerebral hemispheres in delayed BBE. Evans blue was deeply stained in brain stem and hypothalamus in acute BBE comparing to cerebral hemispheres in delayed BBE. These results disclosed that vasomotor paralysis caused by damage and edema of brain stem and hypothalamus to increase cerebral blood volume was responsible for the pathophysiological basis of acute BBE. Delayed BBE was postulated due to cerebral ischemic edema to increase cerebral water content.

关 键 词：脑水肿 病理生理学 减压 脑损伤 

分 类 号：R651.15[医药卫生—外科学]