Sant'Ambrogio F B, Sant'Ambrogio G, Chung K
Departments of Physiology and Biophysics and of Anatomy and Neuroscience, The University of Texas Medical Branch, Galveston, Texas 77555, USA.
J Appl Physiol (1985). 1998 Apr;84(4):1299-304. doi: 10.1152/jappl.1998.84.4.1299.
Gastroesophageal reflux has been indicated as an etiopathological factor in disorders of the upper airway. Upper airway collapsing pressure stimulates pressure-responsive laryngeal receptors that reflexly increase the activity of upper airway abductor muscles. We studied, in anesthetized dogs, the effects of repeated laryngeal instillations of HCl-pepsin (HCl-P; pH = 2) on the response of laryngeal afferent endings and the posterior cricoarytenoid muscle (PCA) to negative pressure. The effect of negative pressure on receptor discharge or PCA activity was evaluated by comparing their response to upper airway (UAO) and tracheal occlusions (TO). It is only during UAO, but not during TO, that the larynx is subjected to negative transmural pressure. HCl-P instillation decreased the rate of discharge during UAO of the 10 laryngeal receptors studied from 56.4 +/- 10.9 (SE) to 38.2 +/- 9.2 impulses/s (P < 0.05). With UAO, the peak PCA moving time average, normalized by dividing it by the peak values of esophageal pressure, decreased after six HCl-P trials from 4.29 +/- 0.31 to 2.23 +/- 0.18 (n = 6; P < 0.05). The responses to TO of either receptors or PCA remained unaltered. We conclude that exposure of the laryngeal mucosa to HCl-P solutions, as it may occur with gastroesophageal reflux, impairs the patency-maintaining mechanisms provided by laryngeal sensory feedback. Inflammatory and necrotic alterations of the laryngeal mucosa are likely responsible for these effects.
胃食管反流已被指出是上呼吸道疾病的一个病因病理因素。上呼吸道塌陷压力刺激压力敏感的喉感受器，从而反射性地增加上呼吸道外展肌的活动。我们在麻醉犬身上研究了反复经喉滴注盐酸胃蛋白酶（HCl-P；pH = 2）对喉传入神经末梢和环杓后肌（PCA）对负压反应的影响。通过比较它们对上呼吸道阻塞（UAO）和气管阻塞（TO）的反应，评估负压对感受器放电或PCA活动的影响。只有在UAO期间，而不是在TO期间，喉部才会受到跨壁负压的影响。在研究的10个喉感受器中，HCl-P滴注使UAO期间的放电率从56.4±10.9（SE）降至38.2±9.2次/秒（P < 0.05）。在UAO时，将PCA移动时间峰值平均值除以食管压力峰值进行归一化处理后，经过6次HCl-P试验，该值从4.29±0.31降至2.23±0.18（n = 6；P < 0.05）。感受器或PCA对TO的反应保持不变。我们得出结论，喉黏膜暴露于HCl-P溶液（如胃食管反流时可能发生的情况）会损害由喉感觉反馈提供的维持通畅的机制。喉黏膜的炎症和坏死改变可能是这些效应的原因。
