Effects of HCl-pepsin laryngeal instillations on upper airway patency-maintaining mechanisms
Effects of HCl-pepsin laryngeal instillations on upper airway patency-maintaining mechanisms
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DOI：
10.1152/jappl.1998.84.4.1299
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发表时间：
1998-04-01
影响因子：
3.3
通讯作者：
Chung, KS
中科院分区：
文献类型：
--
作者：
Sant'Ambrogio, FB;Sant'Ambrogio, G;Chung, KS
胃食管反流已被认为是上呼吸道疾病的一个致病因素。上呼吸道塌陷压力刺激压力反应性喉感受器，反射性地增加上呼吸道外展肌的活动。在麻醉犬的喉部反复灌注盐酸胃蛋白酶（KCl-P; pH = 2）对喉部传入末梢和环杓后肌（PCA）对负压的反应的影响。通过比较它们对上呼吸道（UAO）和气管闭塞（to）的反应，评估负压对受体放电或PCA活性的影响。只有在UAO期间，而不是在TO期间，喉部受到负跨壁压力。HCl-P灌注降低了IO喉受体UAO期间的放电速率，从56.4 +/- 10.9 （SE）降至38.2 +/- 9.2脉冲/s （P < 0.05）。在UAO组中，6次HCl-P试验后，PCA移动时间平均值由4.29 +/- 0.31降至2.23 +/- 0.18 （n = 6, P < 0.05）。受体或PCA对to的反应保持不变。我们的结论是，胃食管反流时，喉粘膜暴露于盐酸- p溶液中，会损害喉感觉反馈提供的通畅维持机制。喉部粘膜的炎症和坏死改变可能是造成这些影响的原因。
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 (KCl-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 IO 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.