Airway responses to esophageal acidification

Abstract

effects of esophageal acidification on airway function are unclear. Some have found that the esophageal acidification causes a small increase in airway resistance, but this change is too small to cause significant symptoms. The aims of this study were to investigate the effects of esophageal acidification on multiple measures of airway function in chloralose-anesthetized cats. The esophagus was cannulated and perfused with either 0.1 M PBS or 0.1 N HCl at 1 ml/min as the following parameters were quantified in separate experiments: diameter of bronchi (n ϭ 5), tracheal mucociliary transport rate (n ϭ 4), tracheobronchial mucus secretion (n ϭ 7), and lung function (n ϭ 6). We found that esophageal acidification for 10 -30 min decreased bronchial diameters primarily of the smaller low-resistance airways (10 -22%, P Ͻ 0.05), decreased tracheal mucociliary transport (53%, 8.7 Ϯ 2.4 vs. 4.1 Ϯ 1.3 mm/min, P Ͻ 0.05), increased tracheobronchial mucus secretion (147%, 3.4 Ϯ 0.7 vs. 8.4 Ϯ 2.6 mg/10 min, P Ͻ 0.05), and caused no change in total lung resistance or dynamic compliance (P Ͼ 0.05). Considering that tracheal mucociliary transport rate is governed in part by mucus secretion, we concluded that the primary airway response to esophageal acidification observed is increased mucus secretion. Airway constriction may act to assist in rapid secretion of mucus and to increase the effectiveness of coughing while not affecting lung resistance or compliance. Given the buffering capabilities of mucus, esophageal acidification activates appropriate physiological responses that may act to neutralize gastroesophageal reflux that reaches the larynx, pharynx, or lower airways. mucociliary transport; gastroesophageal reflux; apocrine gland secretion; airway resistance THE ESOPHAGUS HAS BEEN IMPLICATED as a source of receptors for reflex-induced airway disorders including gastroesophageal reflux-induced asthma (10,18,33,47) and chronic cough (11,22,39); however, the role of the esophagus in airway disorders is unclear. Studies have found that stimulation of the esophagus using HCl (1,2,13,23,32,47,53,59) or mechanical distension (2, 32) caused increased airway resistance (decreased compliance) or tracheal pressure; however, the mechanisms of these responses remain unclear. In all of these studies but one (13), the esophagus was not ligated to prevent esophago-pharyngeal or esophago-laryngeal reflux of the applied acid. Considering that stimulation of the larynx with HCl (23) causes a much greater response of the airways than esophageal stimulation (250 vs. 15% increase in tracheal pressure), it is possible that the airway effects due to esophageal acidification observed in prior studies (1,2,23,39,47,53,59) were due to laryngeal rather than esophageal stimulation. In the one study (13) in which esophago-laryngeal reflux was prevented, the investigators used HCl concentrations (0.3-3.0 N HCl) far above the physiological range, and the effect on airway resistance was small (ϳ10%) and inconsistent. Therefore, no studies of the effects o...

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