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Mechanisms of airway responses to esophageal acidification in cats.
Lang, Ivan M; Haworth, Steven T; Medda, Bidyut K; Forster, Hubert; Shaker, Reza.
Afiliación
  • Lang IM; Dysphagia Institute, Division of Gastroenterology and Hepatology, Medical College of Wisconsin, Milwaukee, Wisconsin; imlang@mcw.edu.
  • Haworth ST; Department of Pulmonary Medicine, Medical College of Wisconsin, Milwaukee, Wisconsin; and.
  • Medda BK; Dysphagia Institute, Division of Gastroenterology and Hepatology, Medical College of Wisconsin, Milwaukee, Wisconsin;
  • Forster H; Department of Physiology, Medical College of Wisconsin, Milwaukee, Wisconsin.
  • Shaker R; Dysphagia Institute, Division of Gastroenterology and Hepatology, Medical College of Wisconsin, Milwaukee, Wisconsin;
J Appl Physiol (1985) ; 120(7): 774-83, 2016 Apr 01.
Article en En | MEDLINE | ID: mdl-26846551
Acid in the esophagus causes airway constriction, tracheobronchial mucous secretion, and a decrease in tracheal mucociliary transport rate. This study was designed to investigate the neuropharmacological mechanisms controlling these responses. In chloralose-anesthetized cats (n = 72), we investigated the effects of vagotomy or atropine (100 µg·kg(-1)·30 min(-1) iv) on airway responses to esophageal infusion of 0.1 M PBS or 0.1 N HCl at 1 ml/min. We quantified 1) diameter of the bronchi, 2) tracheobronchial mucociliary transport rate, 3) tracheobronchial mucous secretion, and 4) mucous content of the tracheal epithelium and submucosa. We found that vagotomy or atropine blocked the airway constriction response but only atropine blocked the increase in mucous output and decrease in mucociliary transport rate caused by esophageal acidification. The mucous cells of the mucosa produced more Alcian blue- than periodic acid-Schiff (PAS)-stained mucosubstances, and the mucous cells of the submucosa produced more PAS- than Alcian blue-stained mucosubstances. Selective perfusion of the different segments of esophagus with HCl or PBS resulted in significantly greater production of PAS-stained mucus in the submucosa of the trachea adjacent to the HCl-perfused esophagus than in that adjacent to the PBS-perfused esophagus. In conclusion, airway constriction caused by esophageal acidification is mediated by a vagal cholinergic pathway, and the tracheobronchial transport response is mediated by cholinergic receptors. Acid perfusion of the esophagus selectively increases production of neutral mucosubstances of the apocrine glands by a local mechanism. We hypothesize that the airway responses to esophageal acid exposure are part of the innate, rather than acute emergency, airway defense system.
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Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Esófago / Pulmón Límite: Animals Idioma: En Revista: J Appl Physiol (1985) Asunto de la revista: FISIOLOGIA Año: 2016 Tipo del documento: Article Pais de publicación: Estados Unidos

Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Esófago / Pulmón Límite: Animals Idioma: En Revista: J Appl Physiol (1985) Asunto de la revista: FISIOLOGIA Año: 2016 Tipo del documento: Article Pais de publicación: Estados Unidos