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J Appl Physiol 84: 1299-1304, 1998;
8750-7587/98 $5.00
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Vol. 84, Issue 4, 1299-1304, April 1998

Effects of HCl-pepsin laryngeal instillations on upper airway patency-maintaining mechanisms

Franca B. Sant'Ambrogio, Giuseppe Sant'Ambrogio, and Kyungsoon Chung

Departments of Physiology and Biophysics and of Anatomy and Neuroscience, The University of Texas Medical Branch, Galveston, Texas 77555

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.

gastroesophageal reflux; laryngeal pressure receptors; upper airway patency; posterior cricoarytenoid muscle; laryngeal mucosa


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