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

自发性脑出血(ICH)约占10% 所有中风的年发病率约为15/10万。当前 治疗结果令人失望。初始死亡率仍然很高，而且 幸存者往往有严重的残废。新疗法 方法很难追寻，因为人们对 脑损伤的病理生理机制。这项研究的目标是 为了确定药物降低平均动脉压是否 在急性脑出血后24小时内产生或加重缺血。我们会 检验特定的零假设：药理降压 15%+5%的自发性幕上脑出血患者未产生 局部脑缺血可能严重到足以引起组织 受伤。我们将执行这一特定目标：30名急性胰腺炎患者 发病24小时内的ICH和初始平均动脉压120-150 刚刚完成局部脑血流量测量的毫米汞柱 (RCBF)，局部脑氧代谢率(RCMRO2)，局部 氧摄取分数(Roef)和脑局部静脉氧 内容(RCvO2)使用正电子发射断层扫描(PET)作为 项目3将被随机分成3组，每组10名患者。一 这些患者将不会接受降压药治疗。第二个和第三个 两组分别接受拉贝洛尔(II组)或尼卡地平(III组)治疗 在60分钟内将平均动脉压降低15正负%。我们将重复PET 在达到目标地图之后的测量，或者对于对照组， 大约60分钟后。我们将确定 药物降低平均大脑半球CBF的MAP，我们还将 确定是否存在从安全到危险或致命的关键转变 RCBF、rCMRO2和rCvO2的范围。这项研究将提供 最基本的重要病理生理学信息 医源性脑缺血在继发性脑损伤中的作用 脑出血患者在规划未来方面将具有巨大价值 治疗性调查。

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.