Cerebral Vasoregulation In Elderly with Stroke

描述(申请人提供)：中风是老年人的第三大致死原因和致残的首要原因。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：老年缺血性中风患者脑血管调节受损，导致脑血流依赖于血压。因此，我们将评估脑血管调节对二氧化碳和血压挑战的反应，以确定卒中高血压患者的脑血流量是否高于卒中正常血压受试者。假设2：中风后自主血压控制发生改变。因此，日常生活活动可能会导致直立性低血压(OH)，构成脑低灌流的风险。我们将评估立位应激期间的脑血流和血压反应，以确定可能发展为脑低灌注的OH受试者。假设3：血管反应性受损的分布从梗塞部位延伸到灰质和白质周围区域，影响不同的血管区域。我们将在3Tesla MRI上使用动脉自旋标记来量化大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磁共振成像来测量梗塞的分布和脑白质的变化，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，卒中后6个月第一个半球大血管梗塞累及大脑中动脉1/3)，并与60名血压正常和高血压但无卒中的受试者进行比较。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大脑中动脉血流速度(BFV)。脑血管对血压刺激的反应性将通过对Valsalva动作、坐立试验和直立倾斜的BFV反应来评估。我们期望发现，随着血管调节受损，脑血流量变得依赖于灌流压力。因此，在中风的老年患者中，羟色胺可能会引发脑低灌流，并对已经受损的脑血管床造成进一步的损害。这项研究的结果可能会提高我们对老年中风患者维持脑血流灌注的最佳血压目标的理解。

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.