School of Physical Education, Sport and Exercise Sciences, University of Otago, Dunedin, New Zealand.
Department of Medicine, Dunedin School of Medicine, University of Otago, Dunedin, New Zealand.
Exp Physiol. 2019 Nov;104(11):1678-1687. doi: 10.1113/EP087832. Epub 2019 Oct 9.
What is the central question of the study? What are the effects of acute mental stress on the mechanisms regulating cerebral blood flow? What is the main finding and its importance? The major new findings are as follows: (i) high mental stress and hypercapnia had an interactive effect on mean middle cerebral artery blood velocity; (ii) high mental stress altered the regulation of cerebral blood flow; (iii) the increased cerebrovascular hypercapnic reactivity was not driven by changes in mean arterial pressure alone; and (iv) this increased perfusion with mental stress appeared not to be justified functionally by an increase in oxygen demand (as determined by near-infrared spectroscopy-derived measures).
In this study, we examined the effects of acute mental stress on cerebrovascular function. Sixteen participants (aged 23 ± 4 years; five female) were exposed to low and high mental stress using simple arithmetic (counting backwards from 1000) and more complex arithmetic (serial subtraction of 13 from a rapidly changing four-digit number), respectively. During consecutive conditions of baseline, low stress and high stress, end-tidal partial pressure of CO ( ) was recorded at normocapnia (37 ± 3 mmHg) and clamped at two elevated levels (P < 0.01): 41 ± 1 and 46 ± 1 mmHg. Mean right middle cerebral artery blood velocity (MCAv ; transcranial Doppler ultrasound), right prefrontal cortex haemodynamics (near-infrared spectroscopy) and mean arterial blood pressure (MAP; finger photoplethysmography) were measured continuously. Cerebrovascular hypercapnic reactivity (ΔMCAv /Δ ), cerebrovascular conductance (CVC; MCAv /MAP), CVC CO reactivity (ΔCVC/Δ ) and total peripheral resistance (MAP/cardiac output) were calculated. Acute high mental stress increased MCAv by 7 ± 7%, and more so at higher (32 ± 10%; interaction, P = 0.03), illustrating increased sensitivity to CO (i.e. its major regulator). High mental stress also increased MAP (17 ± 9%; P ≤ 0.01), coinciding with increased near-infrared spectroscopy-derived prefrontal haemoglobin volume and saturation measures. High mental stress elevated both cerebrovascular hypercapnic and conductance reactivities (main effect of stress, P ≤ 0.04). These findings indicate that the cerebrovascular response to acute high mental stress results in a coordinated regulation between multiple processes.
研究的核心问题是什么？急性心理应激对调节脑血流的机制有什么影响？主要发现及其重要性是什么？主要新发现如下：（i）高心理应激和高碳酸血症对大脑中动脉平均血流速度有交互作用；（ii）高心理应激改变了脑血流的调节；（iii）脑血管的高碳酸反应性增加不仅仅是由平均动脉压的变化引起的；（iv）这种用心理应激增加的灌注在功能上似乎不是由氧需求的增加（通过近红外光谱衍生的测量来确定）来证明是合理的。
在这项研究中，我们研究了急性心理应激对脑血管功能的影响。16 名参与者（年龄 23±4 岁；5 名女性）分别接受简单算术（从 1000 倒数）和更复杂的算术（快速变化的四位数上连续减去 13）的低心理应激和高心理应激暴露。在基础状态、低应激和高应激的连续条件下，在正常碳酸血症（37±3mmHg）和两个升高水平（P<0.01）下记录呼气末二氧化碳分压（ ）：41±1mmHg 和 46±1mmHg。连续测量右大脑中动脉平均血流速度（MCAv；经颅多普勒超声）、右前额叶皮质血液动力学（近红外光谱）和平均动脉血压（MAP；手指光电容积脉搏波）。计算脑血管高碳酸反应性（ΔMCAv/Δ ）、脑血管传导性（CVC；MCAv/MAP）、CVC 二氧化碳反应性（ΔCVC/Δ ）和总外周阻力（MAP/心输出量）。急性高心理应激使 MCAv 增加 7±7%，在更高的 时增加更多（32±10%；交互作用，P=0.03），表明对 CO（即其主要调节剂）的敏感性增加。高心理应激还使 MAP 增加 17±9%（P≤0.01），同时近红外光谱衍生的前额叶血红蛋白体积和饱和度测量值也增加。高心理应激增加了脑血管高碳酸和传导反应性（应激的主要作用，P≤0.04）。这些发现表明，急性高心理应激对脑血管的反应导致多个过程之间的协调调节。
