ESOPHAGEAL SHORTENING INDUCED BY SHORT-TERM INTRALUMINAL ACID PERFUSION IN OPOSSUM - A CAUSE FOR HIATUS-HERNIA

Citation
Wg. Paterson et Dm. Kolyn, ESOPHAGEAL SHORTENING INDUCED BY SHORT-TERM INTRALUMINAL ACID PERFUSION IN OPOSSUM - A CAUSE FOR HIATUS-HERNIA, Gastroenterology, 107(6), 1994, pp. 1736-1740
Citations number
23
Categorie Soggetti
Gastroenterology & Hepatology
Journal title
ISSN journal
00165085
Volume
107
Issue
6
Year of publication
1994
Pages
1736 - 1740
Database
ISI
SICI code
0016-5085(1994)107:6<1736:ESIBSI>2.0.ZU;2-L
Abstract
Background/Aims: Reflux esophagitis and hiatal hernia commonly coexist , yet a cause and effect relationship remains unclear. This study exam ined whether acute acid-induced esophageal injury induces longitudinal esophageal shortening in the opossum model. Methods: Esophageal lengt h was measured continuously using a specially designed strain gauge tr ansducer in anesthetized opossums while the midesophagus was perfused intraluminally with either normal saline or 100 mmol/L HCI. After a st abilization period, the test solution was perfused for 150 minutes. Th e effect of bilateral cervical vagotomy and atropine (60 mu m/kg intra venously) were determined in separate groups. Parallel studies in whic h resting lower esophageal sphincter pressure was measured before and after prolonged intraesophageal acid perfusion were performed. Results : Esophageal acid perfusion induced acute epithelial injury as determi ned histologically. This was associated with significant esophageal sh ortening compared with saline-perfused controls and was not affected b y vagotomy or atropine. In contrast, acid perfusion invariably induced a decrease in resting lower esophageal sphincter pressure. Conclusion s: Acute acid-induced esophageal mucosal injury induces longitudinal e sophageal shortening that does not involve vagal pathways or cholinerg ic neurons. This raises the possibility that esophagitis could contrib ute to the development of hiatal hernia by inducing esophageal long ax is shortening.