title: Bile-induced adenosine triphosphate depletion and mucosal damage during reflux esophagitis.
abstract: BACKGROUND
  This study was designed to investigate the role of bile in a large animal model of acute esophageal reflux disease.
  
  
  METHODS
  An agar electrode was used to measure the transmucosal potential difference of the esophagus in anaesthetized dogs. The vascular permeability index and the epithelial permeability index of the mucosa were evaluated by means of the Evans blue and the sodium-fluorescein clearance method, respectively. The tissue adenosine triphosphate (ATP) level and the myeloperoxidase activity were determined from tissue biopsies, while the degree of mucosal damage was evaluated histologically on a grade 0-100 scale. Group 1 (n = 8) served as saline-treated control; groups 2 (n = 8), 3 (n = 5) and 4 (n = 5) were exposed for 4 h to canine bile alone, to hydrochloric acid + bile, or to hydrochloric acid alone, respectively.
  
  
  RESULTS
  In Groups 2, 3 and 4 the degree of mucosal damage was significantly increased, and a 4-fold elevation in myeloperoxidase activity was observed. The transmucosal potential difference was decreased significantly below the control level, while the vascular and epithelial permeability indices were significantly increased compared with the control values. Bile, but not hydrochloric acid, evoked a significant (40%) decrease in the ATP level of the esophageal tissue.
  
  
  CONCLUSIONS
  We propose that mucosal dysfunction, structural damage and leukocyte invasion during hydrochloric acid-induced esophageal injury are exacerbated by bile-induced changes in tissue ATP concentrations during experimental esophageal reflux disease.
authors.affiliation: Depts. of Surgery and Pathology and Institute of Surgical Research, University of Szeged, Hungary.
authors.forename: K
authors.initials: K
authors.lastname: Szentpáli
authors.forename: J
authors.initials: J
authors.lastname: Kaszaki
authors.forename: L
authors.initials: L
authors.lastname: Tiszlavicz
authors.forename: G
authors.initials: G
authors.lastname: Lázár
authors.forename: A
authors.initials: A
authors.lastname: Balogh
authors.forename: M
authors.initials: M
authors.lastname: Boros
mesh_terms: D000208:Acute Disease; D000255:Adenosine Triphosphate / Q000502:physiology*; D000818:Animals; D001646:Bile / Q000502:physiology*; D004195:Disease Models, Animal; D004285:Dogs; D004942:Esophagitis, Peptic / Q000473:pathology / Q000503:physiopathology*; D005753:Gastric Mucosa / Q000293:injuries* / Q000473:pathology / Q000503:physiopathology*; D005764:Gastroesophageal Reflux / Q000473:pathology / Q000503:physiopathology*; D008928:Mitochondria / Q000502:physiology
chemical_list: D000255:Adenosine Triphosphate