VASOGENIC BRAIN EDEMA IN ISCHEMIC STROKE

缺血性脑卒中血管源性水肿的分子和细胞机制 还有待于充分阐明。缺血性脑组织引发的炎症 损伤可能导致血管源性脑水肿的发展。的 组织急性炎症的主要发现是：（1） 炎症介质;（2）炎症细胞浸润 （多形核细胞和血小板）;和（3）血管损伤， 增加渗透性。所有这些特征在大脑中已经被注意到。 梗塞血管源性脑水肿的假定介质也是 炎症介质。我们建议调查选定的方面， 在大鼠缺血性中风模型中的缺血后炎症反应。 这项建议的主要重点将是激肽-花生四烯酸 级联。我们将描述这个级联反应的激活与以下方面的关系： 脑水肿、蛋白质外渗和多形性腺瘤的演变 细胞浸润细胞和化学介质的作用， 将研究激肽-花生四烯酸级联反应。这个项目的最终目标 建议是开发新的治疗方案，用于治疗缺血性 脑水肿仍然是一个主要的死亡原因在一个星期内 中风发作

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.