Abstract：
Sulfur dioxide (SO2), a common environmental and industrial air pollutant, possesses a potent effect in eliciting cough reflex, but the primary type of airway sensory receptors involved in its tussive action has not been clearly identified. This study was carried out to determine the relative roles of three major types of vagal bronchopulmonary afferents [slowly adapting receptors (SARs), rapidly adapting receptors (RARs), and C-fibers] in regulating the cough response to inhaled SO2. Our results showed that inhalation of SO2 (300 or 600 ppm for 8 min) evoked an abrupt and intense stimulatory effect on bronchopulmonary C-fibers, which continued for the entire duration of inhalation challenge and returned toward the baseline in 1-2 min after resuming room air-breathing in anesthetized and mechanically ventilated mice. In stark contrast, the same SO2 inhalation challenge generated a distinct and consistent inhibitory effect on both SARs and phasic RARs; their phasic discharges synchronized with respiratory cycles during the baseline (breathing room air) began to decline progressively within 1-3 min after the onset of SO2 inhalation, ceased completely before termination of the 8-min inhalation challenge, and then slowly returned toward the baseline after >40 min. In a parallel study in awake mice, inhalation of SO2 at the same concentration and duration as that in the nerve recording experiments evoked cough responses in a pattern and time course similar to that observed in the C-fiber responses. Based on these results, we concluded that stimulation of vagal bronchopulmonary C-fibers is primarily responsible for triggering the cough response to inhaled SO2.NEW & NOTEWORTHY This study demonstrated that inhalation of a high concentration of sulfur dioxide, an irritant gas and common air pollutant, completely and reversibly inhibited the neural activities of both slowly adapting receptor and rapidly adapting receptor, two major types of mechanoreceptors in the lungs with their activities conducted by myelinated fibers. Furthermore, the results of this study suggested that stimulation of vagal bronchopulmonary C-fibers is primarily responsible for triggering the cough reflex responses to inhaled sulfur dioxide.
摘要：
二氧化硫(SO2),一种常见的环境和工业空气污染物，具有引起咳嗽反射的有效作用，但主要类型的气道感觉受体参与其咳嗽作用尚未明确确定。进行这项研究是为了确定三种主要类型的迷走神经支气管肺传入神经[缓慢适应受体（SARs），快速适应受体（RAR），和C纤维]调节对吸入SO2的咳嗽反应。我们的结果表明，吸入SO2（300或600ppm，持续8分钟）会对支气管肺C纤维产生突然而强烈的刺激作用，在吸入攻击的整个持续时间内持续，并在麻醉和机械通气的小鼠恢复室内空气呼吸后的1-2分钟内返回基线。与之形成鲜明对比的是,相同的SO2吸入攻击对SARs和阶段性RARs产生了明显且一致的抑制作用；它们在基线期间与呼吸周期同步的阶段性放电（呼吸室内空气）在SO2吸入开始后1-3分钟内开始逐渐下降，在8分钟吸入攻击后完全停止，然后在>40分钟后缓慢返回基线。在清醒小鼠的平行研究中，以与神经记录实验相同的浓度和持续时间吸入SO2会引起咳嗽反应，其模式和时间过程与C纤维反应相似。基于这些结果,我们得出的结论是，迷走神经支气管肺C纤维的刺激是引发对吸入SO2的咳嗽反应的主要原因。
