OBJECTIVE Esophagitis after total gastrectomy has been associated with biliary and pancreatic reflux into the esophagus. The aim is to clarify the effect of PPI (rabeparazole) on these factors in esophagitis. METHODS Sixteen 8-week old male Wistar rats underwent total gastrectomy and esophagoduodenostomy to induce esophageal reflux of duodenal juice. In 5 rats, the sham operation induced a midline laparotomy alone. One week following surgery, they were treated with control (saline) or PPI (rabeprazole) (30mg/kg) ip. Three weeks after operation, all rats were euthanized and the esophagus was evaluated histologically. Esophageal injury was evaluated by macroscopic and microscopic findings, and expression of COX2 and PGE2. Esophageal washing was aspirated for the evaluation of bile acid activity. RESULTS At 3 weeks after surgery, duodenal reflux induced esophageal erosions and ulcer formation as well as marked thickening of esophageal wall. The macroscopic ulcer score and histological ulcer length were significantly reduced by treatment with rabeprazole. The enhanced expression of COX2 and PGE2 in the control group was also markedly inhibited in the rabeprazole treated group. The bile acid activity in the esophageal lumen was significantly increased in the control group and this increase was significantly inhibited in the rabeprazole treated group. CONCLUSIONS Rabeprazole significantly reduces inflammation and hyperplasia in esophageal mucosa. These results indicate that bile acid, inhibited by rabeprazole, plays an important role in mucosal damage induced by duodenal reflux.