Background/aims: Reflux esophagitis and hiatal hernia commonly coexist, yet a cause and effect relationship remains unclear. This study examined whether acute acid-induced esophageal injury induces longitudinal esophageal shortening in the opossum model.
Methods: Esophageal length was measured continuously using a specially designed strain gauge transducer in anesthetized opossums while the midesophagus was perfused intraluminally with either normal saline or 100 mmol/L HCl. After a stabilization period, the test solution was perfused for 150 minutes. The effect of bilateral cervical vagotomy and atropine (60 microns/kg intravenously) were determined in separate groups. Parallel studies in which 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 determined histologically. This was associated with significant esophageal shortening compared with saline-perfused controls and was not affected by vagotomy or atropine. In contrast, acid perfusion invariably induced a decrease in resting lower esophageal sphincter pressure.
Conclusions: Acute acid-induced esophageal mucosal injury induces longitudinal esophageal shortening that does not involve vagal pathways or cholinergic neurons. This raises the possibility that esophagitis could contribute to the development of hiatal hernia by inducing esophageal long axis shortening.