Department of Physiology, University of Kentucky Medical Center, 800 Rose Street, Lexington, KY 40536, USA.
Am J Respir Crit Care Med. 2012 Jun 1;185(11):1190-6. doi: 10.1164/rccm.201201-0088OC. Epub 2012 Apr 13.
Hyperventilation of hot humid air induces transient bronchoconstriction in patients with asthma; the underlying mechanism is not known. Recent studies showed that an increase in temperature activates vagal bronchopulmonary C-fiber sensory nerves, which upon activation can elicit reflex bronchoconstriction.
This study was designed to test the hypothesis that the bronchoconstriction induced by increasing airway temperature in patients with asthma is mediated through cholinergic reflex resulting from activation of these airway sensory nerves.
Specific airway resistance (SR(aw)) and pulmonary function were measured to determine the airway responses to isocapnic hyperventilation of humidified air at hot (49°C; HA) and room temperature (20-22°C; RA) for 4 minutes in six patients with mild asthma and six healthy subjects. A double-blind design was used to compare the effects between pretreatments with ipratropium bromide and placebo aerosols on the airway responses to HA challenge in these patients.
SR(aw) increased by 112% immediately after hyperventilation of HA and by only 38% after RA in patients with asthma. Breathing HA, but not RA, triggered coughs in these patients. In contrast, hyperventilation of HA did not cause cough and increased SR(aw) by only 22% in healthy subjects; there was no difference between their SR(aw) responses to HA and RA challenges. More importantly, pretreatment with ipratropium completely prevented the HA-induced bronchoconstriction in patients with asthma.
Bronchoconstriction induced by increasing airway temperature in patients with asthma is mediated through the cholinergic reflex pathway. The concomitant increase in cough response further indicates an involvement of airway sensory nerves, presumably the thermosensitive C-fiber afferents.
热湿空气过度通气可导致哮喘患者短暂性支气管收缩；其潜在机制尚不清楚。最近的研究表明，温度升高会激活迷走神经支气管肺 C 纤维感觉神经，这些神经在被激活后可引发反射性支气管收缩。
本研究旨在验证以下假说，即在哮喘患者中，气道温度升高引起的支气管收缩是通过这些气道感觉神经的激活引起的胆碱能反射介导的。
对 6 例轻度哮喘患者和 6 例健康受试者进行了 4 分钟等碳酸过度通气的湿热（49°C；HA）和室温（20-22°C；RA）的研究，以测量气道阻力（SR(aw)）和肺功能，以确定气道对这两种空气的反应。采用双盲设计比较了这些患者在吸入异丙托溴铵和安慰剂气雾剂预处理前后对 HA 挑战的气道反应的影响。
哮喘患者过度通气 HA 后立即引起 SR(aw)增加 112%，而仅增加 38% RA。呼吸 HA 会引发哮喘患者的咳嗽，但不会引发 RA。相反，HA 过度通气不会引起咳嗽，仅使健康受试者的 SR(aw)增加 22%；HA 和 RA 挑战对他们的 SR(aw)反应没有差异。更重要的是，异丙托溴铵预处理完全预防了哮喘患者的 HA 引起的支气管收缩。
哮喘患者气道温度升高引起的支气管收缩是通过胆碱能反射途径介导的。咳嗽反应的同时增加进一步表明气道感觉神经的参与，推测是热敏 C 纤维传入纤维。
