Plourde Annik, Lavoie Kim L, Raddatz Candace, Bacon Simon L
Montreal Behavioural Medicine Centre, CIUSSS-NIM, Hôpital du Sacré-Cœur de Montréal, Canada; Research Centre, CIUSSS-NIM, Hôpital du Sacré-Cœur de Montréal, Canada; Department of Psychology, Université du Québec à Montréal (UQAM), Canada.
Montreal Behavioural Medicine Centre, CIUSSS-NIM, Hôpital du Sacré-Cœur de Montréal, Canada; Research Centre, CIUSSS-NIM, Hôpital du Sacré-Cœur de Montréal, Canada; Department of Exercise Science, Concordia University, Montreal, Canada.
Respir Med. 2017 Jun;127:21-32. doi: 10.1016/j.rmed.2017.03.024. Epub 2017 Mar 28.
Psychological stress has long been suspected to have a deleterious effect on asthma, with acute psychological stress being associated with physiological responses in asthma patients.
The purpose of this systematic review was to provide a narrative synthesis of the impact of acute laboratory psychological stress on physiological responses among asthma patients.
An extensive search was conducted by two independent authors using Pubmed, PsycINFO, PsyArticles and the Cochrane Library electronic databases (up to September 2016). English and French articles which assessed physiological responses during or post-stress and compare them to baseline or pre-stress values were included.
Thirty-two studies met the inclusion criteria. Studies indicated that exposure to active stressors (e.g., arithmetic tasks) was associated with an increase in sympathetic nervous system (SNS) responses, cortisol, and inflammatory responses, but had little effect on the caliber of the bronchi. Exposure to passive stressors (e.g., watching stressful movies or pictures) was also associated with an increase in SNS responses and with mild bronchoconstriction. However, a paucity of data for passive stressors limited conclusions on other measures.
In patients with asthma, both active and passive stressors seem to be associated with an increased activation of the SNS. Passive stressors seem to have a more immediate, deleterious impact on the airways than active stressors, but the latter may be associated with delayed inflammatory driven an asthma exacerbation. Further studies are needed to understand the impact of acute stressors on the physiological mechanisms associated with asthma, particularly HPA and immune markers. Systematic review registration number: CRD42015026431.
长期以来,人们一直怀疑心理压力对哮喘有有害影响,急性心理压力与哮喘患者的生理反应有关。
本系统评价的目的是对急性实验室心理压力对哮喘患者生理反应的影响进行叙述性综合分析。
由两位独立作者使用Pubmed、PsycINFO、PsyArticles和Cochrane图书馆电子数据库(截至2016年9月)进行广泛检索。纳入评估应激期间或应激后生理反应并将其与基线或应激前值进行比较的英文和法文文章。
32项研究符合纳入标准。研究表明,暴露于主动应激源(如算术任务)与交感神经系统(SNS)反应、皮质醇和炎症反应增加有关,但对支气管管径影响不大。暴露于被动应激源(如观看压力大的电影或图片)也与SNS反应增加和轻度支气管收缩有关。然而,被动应激源的数据匮乏限制了对其他指标的结论。
在哮喘患者中,主动和被动应激源似乎都与SNS激活增加有关。被动应激源似乎比主动应激源对气道有更直接、有害的影响,但主动应激源可能与炎症驱动的哮喘发作延迟有关。需要进一步研究以了解急性应激源对与哮喘相关的生理机制的影响,特别是下丘脑-垂体-肾上腺(HPA)和免疫标志物。系统评价注册号:CRD42015026431。