CEREBRAL BLOOD FLOW AFTER SUBARACHNOID HEMORRHAGE

蛛网膜下腔出血后的脑血流

• 批准号: 3413582
• 负责人: ROBERT A SOLOMON
• 金额: $ 30.54万
• 依托单位: COLUMBIA UNIV NEW YORK MORNINGSIDE
• 依托单位国家: 美国
• 财政年份: 1991
• 资助国家: 美国
• 起止时间: 1991-02-01 至 1995-01-31
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/3413582
• 关键词: blood volume; brain disorder chemotherapy; cardiac output; human subject; human therapy evaluation; hypervolemia; neurosurgery; nicardipine; subarachnoid hemorrhage; subarachnoid space; vasospasm

DESCRIPTION: (Investigator's Abstract) Following the rupture of an intracranial aneurysm, a devasting complication is the development of delayed cerebral ischemia due to vasospasm. Clinical investigations have demonstrated that prophylactic intravascular volume expansion may reduce the incidence of delayed cerebral ischemia after subarachnoid hemorrhage (SAH), presumably by improving cerebral blood flow (CBF). However, the relationship of the therapy to changes in CBF has not been adequately determined. This proposal is a clinical physiological study comparing CBF during hypervolemia and normovolemic therapy within the first 2 weeks after aneurysmal SAH. Hemodilution will be the same for both groups. The effect of these two treatments as well as cardiac output, hematocrit, blood pressure, and blood volume on CBF will be determined. A secondary assessment will be made of the change in CBF after institution of hypertensive hypervolemia therapy for delayed cerebral ischemia in both normovolemic and hypervolemia subjects. The sensitivity and specificity of transcranial doppler (TCD) to detect vasospasm and predict changes in CBF will also be determined. These goals will be met by randomizing eligible patients with an acute aneurysmal SAH to receive normovolemic or hypervolemia therapy after surgical clipping of aneurysm. Serial measurements before and after institution of therapy will include 133Xenon CBF, Swan Ganz thermodilution cardiac output, blood pressure, pCO2, temperature, total blood volume, hematocrit, and velocities in proximal middle, anterior, and posterior cerebral arteries by TCD. Subjects in either treatment with hypertensive hypervolemia therapy and the above measurements continued.

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