课题基金 / 基金详情

FOCAL CEREBRAL ISCHEMIA IN ACUTE INTRACEREBRAL HEMORRHAGE

FOCAL CEREBRAL ISCHEMIA IN ACUTE INTRACEREBRAL HEMORRHAGE
急性脑出血引起的局灶性脑缺血
批准号:
6500494
负责人:
WILLIAM J POWERS
金额:
$38.25万
依托单位:
依托单位国家:
美国
项目类别:
财政年份:
2001
资助国家:
美国
项目状态:
已结题
起止时间:
2001-06-01 至 2003-05-31

项目摘要

项目成果

WILLIAM J POWERS的其他基金

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中文摘要
翻译
自发性脑出血(ICH)约占 所有中风的年发病率约为15/100,000。 电流 治疗结果令人失望。 初期死亡率仍然很高, 幸存者往往有严重的残余残疾。 新的治疗 这些方法很难实现,因为人们对这些方法知之甚少。 脑损伤的病理生理机制。 本研究的目的是 为了确定脑缺血作为继发性脑缺血的机制的重要性, 急性ICH患者的组织损伤。 我们将测试具体的 零假设:自发性幕上ICH不会产生局部 脑缺血可能严重到足以导致组织损伤。 我们 将执行此特定目标:我们将测量局部脑血 脑血流(rCBF)、局部脑氧代谢率(rCMRO 2)、局部 氧摄取分数(rOEF)和局部脑静脉氧 60例患者使用正电子发射断层扫描(PE)测定rCvO 2 自发性幕上脑出血 将进行初步测量 在最初的24小时内,并在24-72小时后重复。 我们将 确定局部脑缺血患者的比例 可能严重到足以导致组织损伤,以及这种损伤是如何变化的 在急性脑出血后的最初几天。 这项研究将提供 重要的病理生理学信息, 缺血在脑出血继发性脑损伤中的作用 这将对未来的治疗计划具有巨大的价值, 调查事务所
英文摘要
Spontaneous intracerebral hemorrhage (ICH) comprises approximately 10% of all strokes with an annual incidence of approximately 15/100,000. Current treatment results are disappointing. Initial mortality remains high and survivors often have significant residual disability. New therapeutic approaches are difficult to pursue because little is known about the pathophysiologic mechanisms of brain injury. The goal of this research is to determine importance of cerebral ischemia as a mechanism of secondary tissue damage in human subjects with acute ICH. We will test the specific null hypothesis: Spontaneous supratentorial ICH does not produce regional cerebral ischemia potentially severe enough to cause tissue injury. We will perform this Specific Aim: We will measure regional cerebral blood flow (rCBF), regional cerebral metabolic rate of oxygen (rCMRO2), regional oxygen extraction fraction (rOEF) and regional cerebral venous oxygen content (rCvO2) using positron emission tomography (PE) in 60 patients with spontaneous supratentorial ICH. Initial measurements will be made within the first 24 hours and repeated 24-72 hours later. We will determine the proportion of patients with regional cerebral ischemia potentially severe enough to cause tissue injury and how this changes during the first few days after acute ICH. This research will provide fundamentally important pathophysiologic information about the possible role of ischemia in producing secondary brain injury in patients with ICH which will be of enormous value in planning future therapeutic investigations.
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