Larynx vs. esophagus as reflexogenic sites for acid-induced bronchoconstriction in dogs

Abstract

Bronchoconstriction in asthmatic patients is frequently associated with gastroesophageal reflux. However, it is still unclear whether bronchoconstriction originates from the esophagus or from aspiration of the refluxate into the larynx and larger airway. We compared the effect of repeated esophageal and laryngeal instillations of HCl-pepsin (pH 1.0) on tracheal smooth muscle activity in eight anesthetized and artificially ventilated dogs. Saline was used as control. We used pressure in the cuff of an endotracheal tube (Pcuff) as a direct index of smooth muscle activity at the level of the larger airways controlled by vagal efferents. The Pcuff values of the first 60 s after instillations were averaged, and the difference from the baseline values was evaluated. Changes in Pcuff were significantly greater with laryngeal than with esophageal instillations (P = 0.0166). HCl-pepsin instillation into the larynx evoked greater responses than did saline (P = 0.00543), whereas no differences were detected with esophageal instillations. Repeated laryngeal exposure enhanced the responsiveness significantly (P < 0. 001). Our data indicate that the larynx is more important than the esophagus as a reflexogenic site for the elicitation of reflex bronchoconstriction in response to acidic solutions.

Exhaled breath condensate pH is a robust and reproducible assay of airway acidity

“…Indeed in cats, instillation of 50 mL of 0.2 N hydrochloric acid into the trachea caused a 420% increase in airway resistance [15]. Dogs respond similarly [16].…”

Airway responses to esophageal acidification

“…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.…”

Tachykinins and airway microvascular leakage induced by HCl intra-oesophageal instillation

“…Although instillation of acid in airways produces bronchospasm in animals [6][7], pulmonary aspiration of refluxed stomach content has not been convincingly demonstrated in clinical or scintigraphical studies of large groups of asthmatic patients with gastrooesophageal reflux [8,9].…”