Assessment of the cerebral pressure-flow relationship using psychological stress to manipulate blood pressure
Assessment of the cerebral pressure-flow relationship using psychological stress to manipulate blood pressure
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DOI：
10.1111/psyp.13265
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发表时间：
2018-12-01
期刊：
影响因子：
3.7
通讯作者：
Lucas, Samuel J. E.
中科院分区：
文献类型：
--
作者：
Brindle, Ryan C.;Ginty, Annie T.;Lucas, Samuel J. E.
最近的证据表明，大脑自动调节（CA）可能比以前想象的更加被动。也就是说，传统上认为脑血流量的调节与平均动脉压 (MAP) 无关，但在某种程度上，脑血流量可能会随着 MAP 的变化而波动。然而，由于实验使用药物来操纵 MAP 的局限性以及动脉二氧化碳控制的不一致，关于 MAP 与脑血流关系的问题仍然存在，特别是在改变 MAP 的典型日常活动期间。因此，本研究旨在使用非药物急性心理应激任务来评估 CA，以增强 MAP，同时控制呼气末二氧化碳 (PETCO2)。 25 名健康的年轻人完成了一项有压力的任务，同时记录了 MAP、大脑中动脉血流速度 (MCAv) 和 PETCO2 的连续测量。从分层线性回归获得的斜率值用于评估 MAP-MCAv 关系的强度和 PETCO2 的控制。压力任务显着增加了 MAP (p < 0.001) 和 MCAv (p < 0.001)，并降低了 PETCO2 (p = 0.05)。任务引起的 MAP 每增加 10 mmHg，MCAv 增加约 3.5%；任务引起的 PETCO2 变化并没有明显改变 MAP-MCAv 关系。更大的任务诱导的 MAP 反应与 MAP-MCAv 斜率值降低显着相关，与 CA 一致。这些数据支持 CA 比之前认为的压力被动性更强的假设，并提供初步证据表明压力被动 MAP-MCAv 关系可能在观察到的 MAP 应激反应、中风和脑血管疾病之间的关联中发挥作用。
Recent evidence indicates that cerebral autoregulation (CA) might be more pressure passive than previously thought. That is, cerebral blood flow, traditionally thought to be regulated independently of prevailing mean arterial pressure (MAP), might fluctuate, to some extent, as a function of MAP. However, due to limitations associated with experimental usage of pharmaceuticals to manipulate MAP and inconsistent control of arterial carbon dioxide, questions remain regarding the MAP-cerebral blood flow relationship, especially during typical daily activities that alter MAP. Therefore, the current study aimed to assess CA using a nonpharmacological acute psychological stress task to augment MAP, while at the same time controlling for end-tidal carbon dioxide (PETCO2). Twenty-five healthy young adults completed a stressful task while continuous measures of MAP, middle cerebral artery blood flow velocity (MCAv), and PETCO2 were recorded. Slope values obtained from hierarchical linear regression were used to assess the strength of the MAP-MCAv relationship and control for PETCO2. The stress task significantly increased MAP (p < 0.001) and MCAv (p < 0.001), and decreased PETCO2 (p = 0.05). For every 10 mmHg task-induced increase in MAP, MCAv increased by approximate to 3.5%; task-induced changes in PETCO2 did not appreciably change the MAP-MCAv relationship. Greater task-induced MAP responses were significantly related to decreased MAP-MCAv slope values, consistent with CA. These data support the hypothesis that CA is more pressure passive than previously thought and provide initial evidence indicating that a pressure-passive MAP-MCAv relationship may play a role in the observed associations between MAP stress responses, stroke, and cerebrovascular disease.