BLOOD TO BRAIN SODIUM TRANSPORT IN ISCHEMIC BRAIN EDEMA

缺血性脑水肿中钠的血脑转运

• 批准号: 3407859
• 负责人: A LORRIS BETZ
• 金额: $ 13.27万
• 依托单位: UNIVERSITY OF MICHIGAN AT ANN ARBOR
• 依托单位国家: 美国
• 财政年份: 1987
• 资助国家: 美国
• 起止时间: 1987-04-01 至 1990-03-31
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/3407859
• 关键词: blood brain barrier; blood volume; brain edema; capillary; cerebral ischemia /hypoxia; free radicals; gerbil /jird; laboratory rat; radioassay; steroids; vascular endothelium permeability

Brain edema is a major complication and cause of death following a stroke. The development of ischemic brain edema is related to an increase in the sodium content of the ischemic tissue; however, the mechanisms that lead to this accumulation of sodium are unknown. Previous work from our laboratory has established that sodium crosses the blood-brain barrier by means of specific transport systems which are responsible for secretion of fluid from blood to brain. We postulate that ischemic edema results, in part, from reduced clearance of this secreted fluid. Inhibition of sodium transport across the blood-brain barrier by pharmacologic agents could, therefore, provide a way to limit brain edema formation. The goal is to determine the role of sodium transport at the blood-brain barrier in the development of ischemic brain edema. Two models of cerebral ischemia will be compared: partial unilateral ischemia and complete bilateral ischemia with reperfusion. At various times after these insults, we will quantitate and correlate regional brain edema, tissue content of sodium and potassium, cerebral blood flow rate, brain blood volume, blood-brain barrier integrity, and the rate of transport of sodium from blood to brain. The relationship between blood flow, amount of edema, and rate of sodium uptake will be determined. These studies will improve our understanding of ischemic brain edema and this could ultimately lead to more effective therapy for this important complication of stroke.

脑水肿是中风后的主要并发症和死亡原因。 缺血性脑水肿的发展与增加 缺血组织的钠含量；但是，导致的机制 钠的积累尚不清楚。 我们实验室的先前工作 已经确定钠通过 负责分泌流体的特定运输系统 从血到大脑。 我们假设缺血性水肿结果部分 从清除这种分泌的液体的清除率。 抑制钠 药理学剂穿越血脑屏障的运输可以，可以 因此，提供一种限制大脑水肿形成的方法。 目的是确定钠转运在血脑内的作用 缺血性脑水肿发展的障碍。 两种大脑 将比较缺血：部分单侧缺血并完整 再灌注双侧缺血。 在这些侮辱之后的不同时间， 我们将定量和关联区域脑水肿，组织含量 钠和钾，脑血流量，脑血量， 血脑屏障完整性和钠的运输速率 血向大脑。 血流，水肿量和 将确定钠摄取的速率。 这些研究将提高我们对缺血性脑浮肿的理解和 这最终可能导致对这一重要的更有效的疗法 中风并发症。