Cerebral Vasoregulation In Elderly with Stroke

描述（由申请人提供）：中风是导致老年人死亡和残疾的第三大原因。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脑血管调节功能受损，导致脑血流依赖于血压。因此，我们将评估脑血管对CO2和BP挑战的响应，以确定脑卒中高血压患者的脑血流量是否随着灌注压的增加而高于脑卒中正常受试者。假设2：卒中后自主血压控制发生改变。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。我们将评估直立应激时的脑血流量和血压反应，以识别可能出现脑灌注不足的OH患者。假设3：受损血管反应性的分布超出梗死部位延伸到周围的灰质和白质区域，影响不同的血管区域。我们将在3特斯拉MRI上使用动脉自旋标记来量化脑灰质和白质的血流，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测量梗死的分布和白质变化，并将其与脑血流图进行比较。我们将研究60名受试者（60岁，血压正常和高血压，第一半球大血管梗死影响<1/3的大脑中动脉区域[MCA]，中风后6个月），并将其与60名没有中风的血压正常和高血压受试者进行比较。为了评估血管对二氧化碳刺激的反应性，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两个mca的血流速度（BFV）。脑血管对血压刺激的反应性将通过对Valsalva动作、坐立试验和头向上倾斜的BFV反应来评估。我们期望发现在血管调节受损的情况下，脑血流变得依赖于灌注压。因此，在老年中风患者中，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。本研究的结果可能会提高我们对老年脑卒中患者维持脑灌注的最佳血压目标的认识。

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.