期刊
AMERICAN JOURNAL OF PHYSIOLOGY-REGULATORY INTEGRATIVE AND COMPARATIVE PHYSIOLOGY
卷 301, 期 6, 页码 R1779-R1785出版社
AMER PHYSIOLOGICAL SOC
DOI: 10.1152/ajpregu.00182.2011
关键词
hypoxemia; muscle sympathetic nerve activity; autonomic control
类别
资金
- Natural Sciences and Engineering Research Council of Canada
- Heart and Stroke Foundation of Canada
- Canadian Stroke Network
- Canadian Institutes of Health Research
- Michael Smith Foundation for Health Research
Querido JS, Wehrwein EA, Hart EC, Charkoudian N, Henderson WR, Sheel AW. Baroreflex control of muscle sympathetic nerve activity as a mechanism for persistent sympathoexcitation following acute hypoxia in humans. Am J Physiol Regul Integr Comp Physiol 301: R1779-R1785, 2011. First published September 28, 2011; doi:10.1152/ajpregu.00182.2011.-This study tested the hypothesis that acute isocapnic hypoxia results in persistent resetting of the baroreflex to higher levels of muscle sympathetic nerve activity (MSNA), which outlasts the hypoxic stimulus. Cardiorespiratory measures were recorded in humans (26 +/- 1 yr; n = 14; 3 women) during baseline, exposure to 20 min of isocapnic hypoxia, and for 5 min following termination of hypoxia. The spontaneous baroreflex threshold technique was used to determine the change in baroreflex function during and following 20 min of isocapnic hypoxia (oxyhemoglobin saturation = 80%). From the spontaneous baroreflex analysis, the linear regression between diastolic blood pressure (DBP) and sympathetic burst occurrence, the T50 (DBP with a 50% likelihood of a burst occurring), and DBP error signal (DBP minus the T50) provide indexes of baroreflex function. MSNA and DBP increased in hypoxia and remained elevated during posthypoxia relative to baseline (P < 0.05). The DBP error signal became progressively less negative (i.e., smaller difference between DBP and T50) in the hypoxia and posthypoxia periods (baseline: -3.9 +/- 0.8 mmHg; hypoxia: -1.4 +/- 0.6 mmHg; posthypoxia: 0.2 +/- 0.6 mmHg; P < 0.05). Hypoxia caused no change in the slope of the baroreflex stimulus-response curve; however, there was a shift toward higher pressures that favored elevations in MSNA, which persisted posthypoxia. Our results indicate that there is a resetting of the baroreflex in hypoxia that outlasts the stimulus and provide further explanation for the complex control of MSNA following acute hypoxia.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据