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丘脑重度着色，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。说明：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。
36 cats were divided into 3
groups accord-ing to the duration of global ischemia (flatEEG and no CBF),i.e.acute BBE with
25minutes of ischemia,delayed BBE with 15minutes of ischemia and no BBE with 5 minutsof
ischemia 12 cats were included in eachgroup. 6 cats were sacrificed in the end of ex-periment
for histological examination,and oth-er 6 cats were injected with 2%Evans blue(4mg/kg)and
sacrificed at one hour later(3cats)and the end of experiment.(3 cats) re-spectively.
Histologically, the vascular dam-age,dilation,bleeding and neuronal necrosis were found
prominently in brain stem and hy-pothalamus in acute BBE。 Cerebal ischemicedema was
observed mainly in gray and whitematter of cerebral hemispheres in delayedBBE,Evans blue
was deeply stained in brainstem and hypothalamus in acute BBE compar-ing to cerebral
hemispheres in delayed BBE。These results disclosed that vasomotor paraly-sis caused by
damage and edema of brain stemand hypothalamus to increase cerebral bloodvolume was
responsible for the pathophysi-ological basis of acute BBE。Delayed BBE waspostulated due
to cerebral ischemic edema toincrease cerebral water content。
出处
《中华实验外科杂志》
CAS
CSCD
北大核心
1994年第3期178-179,共2页
Chinese Journal of Experimental Surgery
关键词
脑肿胀
脑水肿
病理生理学
减压
brain edema
pathophysi-ology decompression brain injuries
