HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text Full Text (PDF) All Versions of this Article: 294/1/R211    most recent 00394.2007v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in ISI Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via Google Scholar Google Scholar Articles by Lang, I. M. Articles by Shaker, R. Search for Related Content PubMed PubMed Citation Articles by Lang, I. M. Articles by Shaker, R.

ENVIRONMENTAL, EXERCISE AND RESPIRATORY PHYSIOLOGY

Airway responses to esophageal acidification

Medical College of Wisconsin Dysphagia Institute, Divisions of Gastroenterology and Hepatology and Pulmonary Medicine, Department of Physiology, Medical College of Wisconsin, Milwaukee, Wisconsin

Submitted 6 June 2007 ; accepted in final form 10 October 2007

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.

mucociliary transport; gastroesophageal reflux; apocrine gland secretion; airway resistance