脑出血后脑水肿的发病机制  

The Brain Edema Pathogenesy of Hypertensive Intracerebral Hemorrhage

作　　者：刘培华[1] 范良军[1] 

机构地区：[1]石门县人民医院神经内科,湖南石门415300

出　　处：《医学综述》2009年第20期3126-3128,共3页Medical Recapitulate

摘　　要：高血压性脑出血(HICH)后脑水肿的发生发展是多种因素作用的结果。占位效应、缺血因素、凝血酶在早期脑水肿中起重要作用。红细胞诱发了迟发性脑水肿形成,血红蛋白与血浆蛋白能够诱导脑水肿。HICH后会引起周围脑组织的炎性反应。细胞凋亡机制可能参与了继发性脑组织损伤。血管内皮生长因子、内源性阿片肽、血管活性物质、铁超负荷等也参与了脑水肿的形成。研究HICH后脑水肿发病机制及防治脑水肿对HICH的治疗具有重要的意义。The development on brain edema of hypertensive intracerebral hemorrhage（HICH）is the result of multi-factors.Occupying effect,ischemia and thrombin play an important role in the early brain edema.Red blood corpuscles induce tardive brain edema.Hemoglobin and plasma protein can induce brain edema.Inflammatory reaction of acroteric brain tissues were induced by HICH,cell apoptosis,VEGF,endogenous opioid peptides,vasoactive substance,iron overload,etc.also participate in the emerge of brain edema.It′s very important to research the pathogenesy and the treatment of brain edema for prevention and cure HICH.

关 键 词：高血压性脑出血 脑水肿 发病机制 

分 类 号：R743[医药卫生—神经病学与精神病学]