Brindle Ryan C, Ginty Annie T, Phillips Anna C, Carroll Douglas
School of Sport, Exercise, and Rehabilitation Sciences, University of Birmingham, Birmingham, UK.
Psychophysiology. 2014 Oct;51(10):964-76. doi: 10.1111/psyp.12248. Epub 2014 Jun 13.
A series of meta-analyses was undertaken to determine the contributions of sympathetic and parasympathetic activation to cardiovascular stress reactivity. A literature search yielded 186 studies of sufficient quality that measured indices of sympathetic (n = 113) and/or parasympathetic activity (n = 73). A range of psychological stressors perturbed blood pressure and heart rate. There were comparable aggregate effects for sympathetic activation, as indexed by increased plasma epinephrine and norepinephrine, and shortened pre-ejection period and parasympathetic deactivation, as indexed by heart rate variability measures. Effect sizes varied with stress task, sex, and age. In contrast to alpha-adrenergic blockade, beta-blockade attenuated cardiovascular reactivity. Cardiovascular reactivity to acute psychological stress would appear to reflect both beta-adrenergic activation and vagal withdrawal to a largely equal extent.
进行了一系列的荟萃分析,以确定交感神经和副交感神经激活对心血管应激反应性的影响。文献检索得到了186项质量足够高的研究,这些研究测量了交感神经活动指标(n = 113)和/或副交感神经活动指标(n = 73)。一系列心理应激源扰乱了血压和心率。交感神经激活(以血浆肾上腺素和去甲肾上腺素增加、射血前期缩短为指标)和副交感神经失活(以心率变异性测量为指标)具有相当的总体效应。效应大小随应激任务、性别和年龄而变化。与α-肾上腺素能阻滞剂不同,β-阻滞剂减弱了心血管反应性。心血管对急性心理应激的反应似乎在很大程度上同等地反映了β-肾上腺素能激活和迷走神经撤离。