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脑出血后脑水肿经时变化机制的探讨
引用本文:孟令秋,张淑琴,吴江,杜丹华,王维.脑出血后脑水肿经时变化机制的探讨[J].中风与神经疾病杂志,2004,21(6):496-498.
作者姓名:孟令秋  张淑琴  吴江  杜丹华  王维
作者单位:吉林大学第一医院神经内科,吉林,长春,130021
摘    要:目的 研究脑出血(mtracerebral hemorrhage,ICH)后血肿周围脑水肿与血脑屏障(blood-brain barrier,BBB)随时间变化的机制,从而为预防脑水肿提供依据。方法90只大耳白兔随机分为3组。1组:在立体定向仪下将300μl生理盐水注入兔左侧基底节;2组:注入200μl自身动脉血与100μl生理盐水;3组:注入200μl自身动脉血与100μl水蛭素。每组每时相(6h、12h、24h、48h、72h)各6只兔。脑组织含水量采用干湿重法测量,血脑屏障的通透性测定采用伊文思兰法。结果动脉血组及水蛭素干预组血肿周围脑组织含水量均在48h达到高峰.此后逐步降低。动脉血组伊文思兰(EB)于24h到达高峰,水蛭素干预组伊文思兰(EB)于48h达高峰。结论脑出血后脑水肿是多种因素综合作用的结果。早期可能和血块凝缩、流体静力压有关;至中期时凝血酶是主导因素;后期则主要由于红细胞裂解物的损害。

关 键 词:脑出血  脑水肿  凝血酶  水蛭素  血脑屏障  红细胞裂解物
文章编号:1003-2754(2004)06-0496-03
修稿时间:2004年9月20日

The development of cerebral edema following experimental intracerebral hemorrhage in rabbit
MENG Ling-qiu,ZHANG Shu-qin,WU Jiang,et al..The development of cerebral edema following experimental intracerebral hemorrhage in rabbit[J].Journal of Apoplexy and Nervous Diseases,2004,21(6):496-498.
Authors:MENG Ling-qiu  ZHANG Shu-qin  WU Jiang  
Abstract:Objective To study the development of brain edema formation following experimental intracerebral hemorrhage(ICH) and its relationship with blood-brain barrier (BBB) permeability.Methods 90 rabbits were randomly divided into 3 groups:1.Physiologic saline was steretactically infused into the left basal ganglia.2.Putologous blood with physiologic saline was infused.3.Autologous blood with hirudin was infused.Each group and each time phase(6,12,24,48,72h)involved 6 rabbits respectively.The BBB permeability and brain water content was determined.Results The brain edema was obvious at 6h after ICH,peaked at 48h and gradually extenuate afterwards in the autologous blood group and hirudin group.While BBB permeability was peaked at 24h and 48h respectively in the autologous blood group and hirudin group.Conclusions Although the mechanisms of brain injury after ICH are not fully understood,several mechanisms appear to contribute to edema development.The coagulation cascade,especially thrombin production,plays a major role in early edema formation,and erythrocyte lysis and hemoglobin toxicity contribute to delayed edema development.The results of the present study may suggest a potential clinical approach for the treatment of ICH.
Keywords:Intracerebral hemorrhage  Cerebral edema  Thrombin  Blood-brain barrier  Erythrocyte lysis
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