HUMAN ESOPHAGEAL SECRETION - MUCOSAL RESPONSE TO LUMINAL ACID AND PEPSIN

Citation
Z. Namiot et al., HUMAN ESOPHAGEAL SECRETION - MUCOSAL RESPONSE TO LUMINAL ACID AND PEPSIN, Gastroenterology, 106(4), 1994, pp. 973-981
Citations number
33
Categorie Soggetti
Gastroenterology & Hepatology
Journal title
ISSN journal
00165085
Volume
106
Issue
4
Year of publication
1994
Pages
973 - 981
Database
ISI
SICI code
0016-5085(1994)106:4<973:HES-MR>2.0.ZU;2-F
Abstract
Background/Aims: Although esophageal histology in humans reveals numer ous submucosal mucous glands, their secretion has never been explored. Therefore, we have studied the chemical composition and physical char acteristics of esophageal secretion under the impact of luminal saline , acid, and acid/pepsin solutions. Methods: The esophageal lumen in 21 healthy volunteers was continuously perfused with saline, HCl, or HCl /pepsin. Perfusates were assayed for mucin, protein, and viscosity. In addition, analysis of amino acid and sugar composition of purified es ophageal mucin was performed. Results: Esophageal perfusion with salin e resulted in luminal release of mucin at the rate of 0.23 +/- 0.03 mg .cm-2.min-1. Acid/pepsin solution significantly enhanced luminal relea se of mucin (0.32 +/- 0.03 mg.cm-2.min-1; P < 0.01). HCl/pepsin soluti on also significantly increased the luminal output of protein (P < 0.0 1) and significantly impaired the viscosity of the esophageal perfusat e (P < 0.05). Threonine, serine, and proline were the major amino acid s within the esophageal mucin, whereas galactose was the predominant c arbohydrate. Conclusions: Luminally released esophageal mucin, shown f or the first time in humans, contributes significantly to maintaining the high viscosity of esophageal secretions. Significant increase in t he luminal release of mucin under the impact of acid and pepsin, with subsequent decline of the perfusate viscosity, may indicate that mucin is the major target for gastric acid and pepsin, absorbing the delete rious impact of the gastroesophageal refluxate.