VASOGENIC BRAIN EDEMA IN ISCHEMIC STROKE

缺血性中风中的血管源性脑水肿

• 批准号: 2267321
• 负责人: Chung Y. Hsu
• 金额: $ 18.3万
• 依托单位: WASHINGTON UNIVERSITY
• 依托单位国家: 美国
• 财政年份: 1990
• 资助国家: 美国
• 起止时间: 1990-02-01 至 1995-06-30
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/2267321
• 关键词: acute phase protein; antiinflammatory agents; arachidonate; bradykinin; brain disorder chemotherapy; brain edema; brain injury; cerebral cortex; cerebral ischemia /hypoxia; cytochrome P450; disease /disorder model; eicosanoid metabolism; electrolyte balance; enzyme inhibitors; experimental brain lesion; free radical oxygen; high performance liquid chromatography; inflammation; kallikreins; laboratory rat; leukotrienes; lipoxygenase; medical complication; myeloperoxidase; neutrophil; oxidoreductase inhibitor; phospholipase inhibitor; platelets; prostacyclins; prostaglandin endoperoxide synthase; prostaglandins; radioimmunoassay; reperfusion; superoxide dismutase; thromboxanes; tissue /cell culture; vascular endothelium permeability

The molecular and cellular mechanism of vasogenic edema in ischemic stroke remains to be fully elucidated. Inflammation initiated by ischemic brain injury may contribute to the development of vasogenic brain edema. The major findings in acute inflammation in tissue are: (1) accumulation of inflammatory mediators; (2) infiltration of inflammatory cells (polymorphonuclear cells and platelets); and (3) vascular injury with increased permeability. All these features have been noted in cerebral infarction. The putative mediators of vasogenic brain edema are also inflammatory mediators. We propose to investigate selected aspects of post-ischemic inflammatory reaction in an ischemic stroke model in the rat. The main focus of this proposal will be on the kinin-arachidonic acid cascade. We will characterize the activation of this cascade in relation to the evolution of brain edema, protein extravasation and polymorphonuclear cell infiltration. The roles of cellular and chemical mediators relevant to kinin-arachidonic acid cascade will be studied. The ultimate goal of this proposal is to develop new therapeutic regimens for treatment of ischemic brain edema which remains to be a major cause of death within one week of stroke onset.

缺血性卒中血管源性水肿的分子和细胞机制 仍有待充分阐明。脑缺血引发的炎症反应 损伤可能参与了血管源性脑水肿的发展。这个 急性炎症在组织中的主要表现是：(1)积聚 炎性介质；(2)炎性细胞浸润 多形核细胞和血小板)；(3)血管损伤 渗透性增加。所有这些特征都已经在大脑中被注意到 脑梗塞。推测的血管源性脑水肿的介质也是 炎症介质。我们建议调查选定的几个方面 大鼠缺血性卒中模型中的缺血后炎症反应。 这项提案的主要焦点将是激动素-花生四烯酸 卡斯卡德。我们将从以下几个方面描述该级联的激活 脑水肿、蛋白外渗和中性粒细胞的演变 细胞渗入。相关的细胞和化学介质的作用 将研究激动素-花生四烯酸级联反应。这样做的最终目的是 建议开发治疗缺血性心脏病的新疗法 脑水肿，仍是一周内死亡的主要原因 中风发作。