Graduate School of Engineering, Chiba University , Chiba , Japan.
Cerebrovascular Research Laboratory, Spaulding Rehabilitation Hospital , Boston, Massachusetts.
J Appl Physiol (1985). 2018 Feb 1;124(2):321-329. doi: 10.1152/japplphysiol.00700.2017. Epub 2017 Nov 14.
Postural changes impair the ability of the cerebrovasculature to buffer against dynamic pressure fluctuations, but the mechanisms underlying this impairment have not been elucidated. We hypothesized that autoregulatory impairment may reflect the impact of static central volume shifts on hemodynamic factors other than arterial pressure (AP). In 14 young volunteers, we assessed the relation of fluctuations in cerebral blood flow (CBF) to those in AP, cardiac output, and CO, during oscillatory lower body pressure (LBP) (±20 mmHg at 0.01 and 0.06 Hz) at three static levels (-20, 0, and +20 mmHg). Static and dynamic changes in AP, cardiac output, and CO explained over 70% of the variation in CBF fluctuations. However, their contributions were different across frequencies and levels: dynamic AP changes explained a substantial proportion of the variation in faster CBF fluctuations (partial R = 0.75, standardized β = 0.83, P < 0.01), whereas those in CO explained the largest portion of the variation in slow fluctuations (partial R = 0.43, β = 0.51, P < 0.01). There was, however, a major contribution of slow dynamic AP changes during negative (β = 0.43) but not neutral (β = 0.05) or positive (β = -0.07) LBP. This highlights the differences in contributions of systemic variables to dynamic and static autoregulation and has important implications for understanding orthostatic intolerance. NEW & NOTEWORTHY While fluctuations in blood pressure drive faster fluctuations in cerebral blood flow, overall level of CO and the magnitude of its fluctuations, along with cardiac output, determine the magnitude of slow ones. The effect of slow blood pressure fluctuations on cerebrovascular responses becomes apparent only during pronounced central volume shifts (such as when standing). This underlines distinct but interacting contributions of static and dynamic changes in systemic hemodynamic variables to the cerebrovascular regulation.
姿势变化会损害脑血管缓冲动态压力波动的能力，但这种损害的机制尚未阐明。我们假设自动调节的损害可能反映了静态中心容积变化对除动脉压（AP）以外的血液动力学因素的影响。在 14 名年轻志愿者中，我们在三个静态水平（-20、0 和 +20mmHg）下评估了振荡性下体压力（LBP）（0.01 和 0.06Hz 时为±20mmHg）期间脑血流（CBF）波动与 AP、心输出量和 CO 波动之间的关系。AP、心输出量和 CO 的静态和动态变化解释了 CBF 波动变化的 70%以上。然而，它们在不同频率和水平下的贡献不同：动态 AP 变化解释了较快 CBF 波动变化的很大一部分（部分 R=0.75，标准化β=0.83，P<0.01），而 CO 的变化解释了较慢波动变化的最大部分（部分 R=0.43，β=0.51，P<0.01）。然而，在负向 LBP（β=0.43）而不是中性（β=0.05）或正向 LBP（β=-0.07）期间，AP 缓慢动态变化的贡献很大。这突出了系统变量对动态和静态自动调节的贡献差异，对于理解直立不耐受具有重要意义。新的和值得注意的是，虽然血压波动会驱动更快的脑血流波动，但 CO 的整体水平及其波动幅度，以及心输出量，决定了缓慢波动的幅度。只有在明显的中心容积转移（如站立时）期间，AP 缓慢波动对脑血管反应的影响才变得明显。这强调了系统血液动力学变量的静态和动态变化对脑血管调节的不同但相互作用的贡献。
