ARTERIAL PRESSURE ON CEREBRAL BLOOD FLOW/OXYGENATION--INTRACEREBRAL HEMORRHAGE

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 以确定药物降低平均动脉压是否 在急性ICH产生或加重缺血后24小时内。 我们将 检验特定的零假设：药物降压 15 ± 5%的自发性幕上ICH患者不会产生 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：30例急性 发病24小时内ICH，初始平均动脉压120-150 mm Hg，刚刚完成局部脑血流量测量 局部脑氧代谢率（rCMRO 2），局部脑血流量（rCBF） 氧摄取分数（rOEF）和局部脑静脉氧 使用正电子发射断层扫描（PET）作为 项目3将随机分为3组，每组10例患者。 一 各组将不接受抗高血压药物治疗。 第二和第三 组将接受拉贝洛尔（组II）或尼卡地平（组III） 在60分钟内使MAP降低15% 我们将重复PET 在达到目标MAP后进行测量，或者对于对照组， 大约60分钟后。 我们将确定 平均半球CBF的MAP药理学降低，我们还将 确定是否有从安全到危险或致命的关键转变 rCBF、rCMRO 2和rCvO 2的范围。 这项研究将提供 重要的病理生理学信息， 医源性脑缺血在继发性脑损伤中的作用 这将对未来的计划具有巨大的价值 治疗研究。

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 whether pharmacologic reduction in mean arterial pressure within 24 hours after acute ICH produces or exacerbates ischemia. We will test the specific null hypothesis: Pharmacologic blood pressure reduction of 15+5% in patients with spontaneous supratentorial ICH does not produce regional cerebral ischemia potentially severe enough to cause tissue injury. We will perform this Specific Aim: Thirty patients with acute ICH within 24 hours of onset and initial mean arterial pressure of 120-150 mm Hg who have just completed measurements of 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 (PET) as part of Project 3 will be randomized into 3 groups of 10 patients each. One groups will receive no antihypertensive medication. The second and third groups will receive either labetalol (Group II) or nicardipine (Group III) to lower MAP by 15 plus minus % within 60 minutes. We will repeat PET measurements after target MAP is reached or, for the control group, approximately 60 minutes later. We will determine the effect of pharmacologic reduction in MAP on average hemispheric CBF and we will also determine if there re critical shifts from safe to dangerous or lethal ranges of rCBF, rCMRO2 and rCvO2. This research will provide fundamentally important pathophysiologic information about the possible role of iatrogenic ischemic in producing secondary brain injury in patients with ICH which will be of enormous value in planning future therapeutic investigations.