title: Esophageal injury with external esophageal perfusion.
abstract: BACKGROUND
  External esophageal perfusion (EEP) with the idea that esophageal perfusion can be controlled with a single ingredient at a constant rate and concentration, might be used to dissect the injurious role of gastro-duodenal secretions for the progression from esophagitis to Barrett's esophagus (BE) and esophageal adenocarcinoma (EAC). This study is to evaluate the EEP rat model for esophagitis induced by using a micro-osmotic pump with bile perfusion.
  
  
  METHODS
  Eighteen adult rats underwent the EEP procedure. Bile (0.5% bovine bile, pH 7.4) was used as perfusion agent and three types of perfusions were performed: 1 week perfusion, 2 weeks perfusion, and 4 weeks perfusion compared to saline perfusion and sham operation. Histological changes, cell proliferation, apoptosis, 8-hydroxy-deoxyguanosine (8-OH-dG) and Manganese superoxide dismutase (MnSOD) were observed after perfusion and compared.
  
  
  RESULTS
  The bile perfusion for 1 week, 2 weeks, and 4 weeks induced mucosa infiltration of inflammatory cells, basal cell hyperproliferation, and papillae hypertrophy in all animals. Histopathology and cellular changes consistent with the findings associated with reflux esophagitis. The apoptotic index, the proliferating index, and expression of 8-OH-dG were significantly increased in the esophageal mucosa compared to controls. MnSOD expression was decreased with bile perfusion compared to saline controls.
  
  
  CONCLUSIONS
  The external esophageal perfusion model enabled precise control of the injurious agent. It induced the typical histological injury and cellular changes seen in severe reflux esophagitis. The cellular changes in apoptosis, proliferation and anti-oxidant defense make this model unique for reflux esophagitis studies. Further studies are needed to induce Barrett's esophagus and esophageal adenocarcinoma.
authors.affiliation: Division of Surgical Oncology, University of Louisville School of Medicine, Louisville, Kentucky 40202, USA.
authors.forename: Yan
authors.initials: Y
authors.lastname: Li
authors.forename: John M
authors.initials: JM
authors.lastname: Wo
authors.forename: Ruifeng R
authors.initials: RR
authors.lastname: Su
authors.forename: Mukunda B
authors.initials: MB
authors.lastname: Ray
authors.forename: Whitney
authors.initials: W
authors.lastname: Jones
authors.forename: Robert C G
authors.initials: RC
authors.lastname: Martin
mesh_terms: D000080242:8-Hydroxy-2'-Deoxyguanosine; D000818:Animals; D017209:Apoptosis; D001646:Bile / Q000737:chemistry; D002455:Cell Division; D003849:Deoxyguanosine / Q000031:analogs & derivatives / Q000032:analysis; D004942:Esophagitis, Peptic / Q000473:pathology*; D004947:Esophagus / Q000737:chemistry / Q000473:pathology*; D005750:Gastric Juice / Q000737:chemistry; D006984:Hypertrophy; D007150:Immunohistochemistry; D020287:In Situ Nick-End Labeling; D009092:Mucous Membrane / Q000473:pathology; D010477:Perfusion; D051381:Rats; D017207:Rats, Sprague-Dawley; D013482:Superoxide Dismutase / Q000032:analysis; D013997:Time Factors
chemical_list: D000080242:8-Hydroxy-2'-Deoxyguanosine; D013482:Superoxide Dismutase; D003849:Deoxyguanosine