AUTOREGULATION OF CEREBRAL BLOOD FLOW IN ACUTE ISCHEMIA

急性缺血时脑血流的自动调节

• 批准号: 6795650
• 负责人: WILLIAM J POWERS
• 金额: $ 24.57万
• 依托单位: WASHINGTON UNIVERSITY
• 依托单位国家: 美国
• 财政年份: 2003
• 资助国家: 美国
• 起止时间: 2003-08-15 至 2008-05-31
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/6795650
• 关键词: acute disease /disorder; antihypertensive agents; blood pressure; brain disorder diagnosis; brain edema; cerebral hemorrhage; cerebral ischemia /hypoxia; clinical research; human subject; human therapy evaluation; magnetic resonance imaging; medical complication; neurologic manifestations; neuroregulation; outcomes research; pathologic process; positron emission tomography; relapse /recurrence; stroke; vascular resistance

Hypertension is one of the most significant risk factors for ischemic stroke. Long term treatment of hypertension after stroke has been shown to reduce the incidence of recurrent stroke by 28% and major cardiovascular complications by 26%. However, in the setting of acute ischemic stroke it has been difficult to determine the appropriate treatment of elevated blood pressure due to the overwhelming concern that lowering blood pressure in this setting might worsen cerebral ischemia. These concerns are based primarily on studies of CBF in animal models. Very few studies of the effect of pharmacological reduction of elevated blood pressure on CBF following acute ischemic stroke in humans have been done and they do not provide adequate data to settle this issue. The goal of this research project is to determine the effect of controlled, graded pharmacologic reduction of blood pressure on rCBF following acute ischemic stroke using positron emission tomography (PET) and to carefully monitor the clinical effects and safety of treatment. This specific null hypothesis will be tested: Pharmacological reduction of mean arterial blood pressure (MAP) by 15 +/- 5 mm Hg in patients with a recent cerebral infarction and elevated blood pressure does not produce a statistically significant reduction in regional cerebral blood flow. This Specific Aim will be carried out: Between day 3-14 after onset, sixty patients with a hemispheric cerebral infarction and mean arterial blood pressure of 120-150 mm Hg will undergo a detailed neurological examination and measurements of rCBF, regional cerebral metabolic rate (rCMRO2), and regional oxygen extraction fraction (rOEF) using PET. Blood pressure will then be lowered pharmacologically in two steps of 7.5 +/- 5 mm Hg each using intravenous labetalol. The neurological examination and CBF measurements will be repeated after each step. This study is not designed to provide data on whether blood pressure in the acute setting improves outcome. This can only be done by randomized treatment trials with clinical outcome measures. These data can, however, be used to help design such a trial and, in the meantime, provide helpful guidelines when reduction in arterial pressure is deemed to be necessary for other reasons. This study will provide esssential information necessary to translate data from animal studies into treatment for human cerebrovascular disease.

高血压是缺血性脑卒中最重要的危险因素之一。中风后长期治疗高血压已被证明可将卒中复发发生率降低28%，将主要心血管并发症发生率降低26%。然而，在急性缺血性脑卒中的情况下，由于普遍担心在这种情况下降低血压可能会加重脑缺血，因此很难确定血压升高的适当治疗方法。这些担忧主要基于动物模型中脑血流的研究。很少有关于人类急性缺血性卒中后血压升高的药理降低对CBF的影响的研究，他们没有提供足够的数据来解决这个问题。这个研究项目的目标是确定控制，