Department of Psychology, University of Hamburg, Hamburg, Germany.
J Appl Physiol (1985). 2010 Jun;108(6):1542-9. doi: 10.1152/japplphysiol.00818.2009. Epub 2010 Apr 1.
In asthma, airways constrict in response to emotion and stress, but underlying mechanisms, potential extrathoracic contributions, and associations with airway pathophysiology have not been elucidated. We therefore investigated the role of the cholinergic pathway in emotion-induced airway responses in patients with asthma and the association of these responses with airway pathophysiology. Patients with asthma (n=54) and healthy participants (n=25) received either 40 microg ipratropium bromide or a placebo in a double-blind double-dummy cross-over design in two laboratory sessions with experimental emotion induction. Stimuli were preevaluated films and pictures of pleasant, unpleasant, and neutral quality. Respiratory resistance and reactance at 5 and 20 Hz were measured continuously before and during presentations, together with respiration by impedance plethysmography and end-tidal PCO2 by capnometry. In addition, measures of airway inflammation (fraction of exhaled nitric oxide), airway hyperreactivity (methacholine challenge), and reversibility of obstruction were obtained. Respiratory resistance at 5 and 20 Hz increased during unpleasant stimuli in asthma patients. This response was blocked by ipratropium bromide and was not substantially associated with asthma severity, airway inflammation, hyperreactivity and reversibility, or pattern of ventilation and PCO2. Under the placebo condition, changes in resistance during unpleasant films were positively correlated with patients' reports of psychological asthma triggers. In conclusion, airway constriction to unpleasant stimuli in asthma depends on an intact cholinergic pathway, is largely due to the central airways, and is not substantially associated with other indicators of airway pathology. Its link to the perceived psychological triggers in patients' daily lives suggests a physiological basis for emotion-induced asthma.
在哮喘中，气道会对情绪和压力作出反应而收缩，但潜在的机制、潜在的胸外贡献以及与气道病理生理学的关联尚未阐明。因此，我们研究了胆碱能通路在哮喘患者情绪诱导的气道反应中的作用，以及这些反应与气道病理生理学的关联。在两个实验室会议中，哮喘患者（n=54）和健康参与者（n=25）接受了 40 微克异丙托溴铵或安慰剂的双盲双模拟交叉设计。刺激物是预先评估的电影和图片，分为愉快、不愉快和中性质量。在呈现之前和期间，通过阻抗体描记术连续测量呼吸阻力和电抗在 5 和 20 Hz 时的变化，并通过呼吸测量呼吸和呼气末 PCO2 通过二氧化碳描记术。此外，还获得了气道炎症（呼出的一氧化氮分数）、气道高反应性（乙酰甲胆碱挑战）和阻塞可逆性的测量值。在哮喘患者中，5 和 20 Hz 时的呼吸阻力在不愉快刺激时增加。这种反应被异丙托溴铵阻断，与哮喘严重程度、气道炎症、高反应性和可逆性、或通气和 PCO2 模式没有实质性关联。在安慰剂条件下，不愉快电影期间阻力的变化与患者报告的心理哮喘触发因素呈正相关。总之，哮喘患者对不愉快刺激的气道收缩依赖于完整的胆碱能通路，主要是由于中央气道，与其他气道病理指标没有实质性关联。它与患者日常生活中感知到的心理触发因素之间的联系表明了情绪诱发哮喘的生理基础。
