Experience with the transthoracic approach to the repair of sliding esophageal hiatal hernia has demonstrated that adequate anatomic repair is not consistently followed by amelioration of symptoms. Further studies of several of these unsuccessfully treated patients have revealed the hitherto undetected presence of high levels of gastric acid secretion not infrequently accompanied by duodenal ulcer. Analysis of large groups of patients with duodenal ulcer and with esophageal hiatal hernia has emphasized the striking similarity of symptoms presented by both groups of patients: retrosternal and subxiphoid pain and burning, regurgitation, pyrosis, flatulence, vomiting, and bleeding. This clinical evaluation pointed to a common pathophysiologic mechanism for the production of symptoms, and the studies herein reported were undertaken to evaluate the nature of the mechanism. It is well known that the presence of a sliding esophageal hernia is not necessarily associated with symptoms. The question may validly be proposed: is the dislocation of