title: Airway responses to esophageal acidification.
abstract: The 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 = 5), tracheal mucociliary transport rate (n = 4), tracheobronchial mucus secretion (n = 7), and lung function (n = 6). We found that esophageal acidification for 10-30 min decreased bronchial diameters primarily of the smaller low-resistance airways (10-22%, P < 0.05), decreased tracheal mucociliary transport (53%, 8.7 +/- 2.4 vs. 4.1 +/- 1.3 mm/min, P < 0.05), increased tracheobronchial mucus secretion (147%, 3.4 +/- 0.7 vs. 8.4 +/- 2.6 mg/10 min, P < 0.05), and caused no change in total lung resistance or dynamic compliance (P > 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.
authors.affiliation: Medical College of Wisconsin Dysphagia Institute, Divisions of Gastroenterology and Hepatology and Pulmonary Medicine, Department of Physiology, Medical College of Wisconsin, Milwaukee, WI 53226, USA. imlang@mcw.edu
authors.forename: Ivan M
authors.initials: IM
authors.lastname: Lang
authors.forename: Steven T
authors.initials: ST
authors.lastname: Haworth
authors.forename: Bidyut K
authors.initials: BK
authors.lastname: Medda
authors.forename: David L
authors.initials: DL
authors.lastname: Roerig
authors.forename: Hubert V
authors.initials: HV
authors.lastname: Forster
authors.forename: Reza
authors.initials: R
authors.lastname: Shaker
mesh_terms: D000403:Airway Resistance / Q000187:drug effects / Q000502:physiology; D000818:Animals; D001980:Bronchi / Q000187:drug effects / Q000473:pathology / Q000503:physiopathology; D002415:Cats; D004195:Disease Models, Animal; D004947:Esophagus / Q000187:drug effects / Q000502:physiology*; D005260:Female; D005764:Gastroesophageal Reflux / Q000473:pathology / Q000503:physiopathology; D006851:Hydrochloric Acid / Q000494:pharmacology*; D006863:Hydrogen-Ion Concentration; D008297:Male; D009079:Mucociliary Clearance / Q000187:drug effects / Q000502:physiology; D009093:Mucus / Q000378:metabolism; D012137:Respiratory System / Q000187:drug effects / Q000378:metabolism / Q000503:physiopathology*
chemical_list: D006851:Hydrochloric Acid