Cerebral Vasoregulation In Elderly with Stroke

描述（由申请人提供）：中风是老年人死亡的第三大原因和残疾的主要原因。我们的长期目标是确定中风对脑血管调节的影响。我们的假设如下：假设1：老年缺血性脑卒中患者的脑血管调节功能受损，使脑血流依赖于血压（BP）。因此，我们将评估脑血管调节对CO2和BP挑战的反应，以确定脑血流量是否高于脑卒中高血压受试者的脑血流灌注压增加。假设2：中风后自主BP控制发生改变。因此，日常生活活动可能诱发直立性低血压（OH），造成脑灌注不足的风险。我们将评估立位应激时的脑血流量和血压反应，以识别可能发生脑灌注不足的OH受试者。假设三：血管反应性受损的分布超出梗死部位，进入周围的灰色和白色物质区域，影响不同的血管区域。我们将在3特斯拉MRI下使用动脉自旋标记定量灰质和白色物质中的脑血流量，并评估低碳酸血症和高碳酸血症期间血管反应性的分布。我们将使用T2加权FLAIR MRI测量梗死和白色物质变化的分布，并将其与脑血流图进行比较。我们将研究60名受试者（>60岁，正常血压和高血压伴第一半球大血管梗死影响<1/3大脑中动脉区域[MCA]，卒中后>6个月），并将其与60名正常血压和高血压无卒中受试者进行比较。为了评价对CO2刺激的血管反应性，我们将使用经颅多普勒超声测量低碳酸血症和高碳酸血症期间MCA中的血流速度（BFV）。将根据BFV对Valsalva动作、坐立试验和头高位倾斜的反应评价对BP刺激的脑血管反应性。我们希望发现，血管调节受损的脑血流变得依赖于灌注压。因此，在患有中风的老年人中，OH可能引发脑灌注不足，并对已经受损的脑血管床造成进一步损害。这项研究的结果可能会提高我们对维持老年脑卒中患者脑灌注的最佳BP目标的理解。

DESCRIPTION (provided by applicant): Stroke is the third leading cause of death and the leading cause of disability in older people. Our long-term goal is to determine the effects of stroke on cerebral vasoregulation. Our hypotheses are as follows: Hypothesis 1: The older adults with ischemic stroke have impaired cerebral vasoregulation, rendering cerebral blood flow dependent on blood pressure (BP). Therefore, we will evaluate cerebral vasoregulation in response to CO2 and BP challenges to determine whether cerebral blood flow is higher with increased perfusion pressure in stroke-hypertensive than stroke-normotensive subjects. Hypothesis 2: Autonomic BP control is altered after stroke. Therefore, activities of daily living may induce orthostatic hypotension (OH), posing a risk of cerebral hypoperfusion. We will evaluate cerebral blood flow and BP responses during orthostatic stress to identify subjects with OH, who may develop cerebral hypoperfusion. Hypothesis 3: The distribution of impaired vasoreactivity extends beyond the infarct site into surrounding areas of gray and white matter affecting different vascular territories. We will quantify cerebral blood flow in gray and white matter using arterial spin labeling at 3 Tesla MRI and evaluate the distribution of vasoreactivity during hypo-and hypercapnia. We will use T2-weighted FLAIR MRI to measure the distribution of infarcts and white matter changes and compare it to the cerebral blood flow maps. We will study 60 subjects (>60 years old, normotensive and hypertensive with the first hemispheric large vessel infarct affecting <1/3 of middle cerebral artery territory [MCA], >6 months post-stroke) and compare them to 60 normotensive and hypertensive subjects without stroke. To evaluate vasoreactivity to CO2 stimulus we will measure blood flow velocity (BFV) in both MCAs during hypo- and hypercapnia using transcranial Doppler ultrasound. Cerebral vasoreactivity to BP stimulus will be evaluated from BFV responses to Valsalva maneuver, sit-to-stand test and head-up tilt. We expect to find that with impaired vasoregulation cerebral blood flow becomes dependent on perfusion pressure. Therefore, in older adults with stroke, OH may trigger cerebral hypoperfusion and cause further damage to an already compromised cerebrovascular bed. The results of this study may improve our understanding of optimal BP targets for the maintenance of cerebral perfusion in elderly people with stroke.