{"title":"740.雷贝拉唑对大鼠胆汁引起的反流性食管炎有保护作用","authors":"Naoki Hashimoto","doi":"10.1093/dote/doae057.353","DOIUrl":null,"url":null,"abstract":"Aims we studied the effect of proton pump inhibitor(PPI)(Rabeprazole) therapy on esophageal bile reflux in esophagitis after total gastrectomy. (Methodology) Sixteen 8-week old male Wistar rats were underwent total gastrectomy and esophagoduodenostomy to induce esophageal reflux of biliary and pancreatic juice. In 5 rats the sham operation induced a midline laparatomy alone (Sham). One week following surgery, they were treated with saline (Control) (n=8) PPI (Rabeprazole)(n=8)(30mg/kg/day) ip for 2 weeks. 3 weeks after operation, all rats were killed and the esophagus was evaluated histologically. Esophageal injury was evaluated by macroscopic, microscopic findings and expression of COX2 and PGE2. We performed the measurement of bile acid in the esophageal lumen and common bile duct. Results At 3 weeks after surgery, duodenal reflux induced esophageal erosions and ulcer formation. The macroscopic ulcer score and microscopic ulcer length were significantly reduced by PPI. The enhanced expression of COX2 and PGE2 in the control group was also markedly inhibited in the PPI group. Really, there is no difference between control group and PPI group in bile acid concentration from the common bile duct. PPI does not inhibit the secretion of bile acid from the common bile duct. But, the bile acid activity in the esophageal lumen was significantly increased in the control group, and this increase was significantly inhibited in the PPI group. Conclusion These results indicate that bile acid, which is inhibited by Rabeprazole, plays an important role in the mucosal damage induced by duodenal reflux.","PeriodicalId":11354,"journal":{"name":"Diseases of the Esophagus","volume":"6 1","pages":""},"PeriodicalIF":2.3000,"publicationDate":"2024-09-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"740. RABEPRAZOLE PROTECTS REFLUX ESOPHAGITIS DUE TO BILE IN RAT MODEL\",\"authors\":\"Naoki Hashimoto\",\"doi\":\"10.1093/dote/doae057.353\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"Aims we studied the effect of proton pump inhibitor(PPI)(Rabeprazole) therapy on esophageal bile reflux in esophagitis after total gastrectomy. (Methodology) Sixteen 8-week old male Wistar rats were underwent total gastrectomy and esophagoduodenostomy to induce esophageal reflux of biliary and pancreatic juice. In 5 rats the sham operation induced a midline laparatomy alone (Sham). One week following surgery, they were treated with saline (Control) (n=8) PPI (Rabeprazole)(n=8)(30mg/kg/day) ip for 2 weeks. 3 weeks after operation, all rats were killed and the esophagus was evaluated histologically. Esophageal injury was evaluated by macroscopic, microscopic findings and expression of COX2 and PGE2. We performed the measurement of bile acid in the esophageal lumen and common bile duct. Results At 3 weeks after surgery, duodenal reflux induced esophageal erosions and ulcer formation. The macroscopic ulcer score and microscopic ulcer length were significantly reduced by PPI. The enhanced expression of COX2 and PGE2 in the control group was also markedly inhibited in the PPI group. Really, there is no difference between control group and PPI group in bile acid concentration from the common bile duct. PPI does not inhibit the secretion of bile acid from the common bile duct. But, the bile acid activity in the esophageal lumen was significantly increased in the control group, and this increase was significantly inhibited in the PPI group. Conclusion These results indicate that bile acid, which is inhibited by Rabeprazole, plays an important role in the mucosal damage induced by duodenal reflux.\",\"PeriodicalId\":11354,\"journal\":{\"name\":\"Diseases of the Esophagus\",\"volume\":\"6 1\",\"pages\":\"\"},\"PeriodicalIF\":2.3000,\"publicationDate\":\"2024-09-02\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Diseases of the Esophagus\",\"FirstCategoryId\":\"3\",\"ListUrlMain\":\"https://doi.org/10.1093/dote/doae057.353\",\"RegionNum\":3,\"RegionCategory\":\"医学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"Q3\",\"JCRName\":\"GASTROENTEROLOGY & HEPATOLOGY\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Diseases of the Esophagus","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.1093/dote/doae057.353","RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q3","JCRName":"GASTROENTEROLOGY & HEPATOLOGY","Score":null,"Total":0}
740. RABEPRAZOLE PROTECTS REFLUX ESOPHAGITIS DUE TO BILE IN RAT MODEL
Aims we studied the effect of proton pump inhibitor(PPI)(Rabeprazole) therapy on esophageal bile reflux in esophagitis after total gastrectomy. (Methodology) Sixteen 8-week old male Wistar rats were underwent total gastrectomy and esophagoduodenostomy to induce esophageal reflux of biliary and pancreatic juice. In 5 rats the sham operation induced a midline laparatomy alone (Sham). One week following surgery, they were treated with saline (Control) (n=8) PPI (Rabeprazole)(n=8)(30mg/kg/day) ip for 2 weeks. 3 weeks after operation, all rats were killed and the esophagus was evaluated histologically. Esophageal injury was evaluated by macroscopic, microscopic findings and expression of COX2 and PGE2. We performed the measurement of bile acid in the esophageal lumen and common bile duct. Results At 3 weeks after surgery, duodenal reflux induced esophageal erosions and ulcer formation. The macroscopic ulcer score and microscopic ulcer length were significantly reduced by PPI. The enhanced expression of COX2 and PGE2 in the control group was also markedly inhibited in the PPI group. Really, there is no difference between control group and PPI group in bile acid concentration from the common bile duct. PPI does not inhibit the secretion of bile acid from the common bile duct. But, the bile acid activity in the esophageal lumen was significantly increased in the control group, and this increase was significantly inhibited in the PPI group. Conclusion These results indicate that bile acid, which is inhibited by Rabeprazole, plays an important role in the mucosal damage induced by duodenal reflux.