title: Luminal ammonia retards restitution of guinea pig injured gastric mucosa in vitro.
abstract: The present study was conducted to elucidate the mechanisms by which Helicobacter pylori (HP)-derived ammonia causes gastric mucosal injury. Intact sheets of guinea pig gastric fundic mucosae were incubated in Ussing chambers. Both the luminal and the serosal pH were kept at 7.4. Transmucosal potential difference (PD) and electrical resistance (R) were monitored as indices of mucosal integrity. Restitution was evaluated by recovery of PD, R, and transmucosal [(3)H]mannitol flux after Triton X-100-induced mucosal injury. The effects of luminal or serosal NH(4)Cl on function and morphology of uninjured or injured mucosae were examined. In uninjured mucosae, serosal NH(4)Cl induced more profound decreases in PD and R and more prominent vacuolation in gastric epithelial cells than did luminal NH(4)Cl. In contrast, luminal NH(4)Cl markedly inhibited restitution in injured mucosae and caused an extensive vacuolation in gastric epithelial cells, as did serosal NH(4)Cl. Transmucosal ammonia flux was greater in the injured than in the uninjured mucosae. These results suggest that 1) basolateral membrane of gastric epithelial cells is more permeable to ammonia than apical membrane and 2) luminal ammonia, at concentrations detected in HP-infected gastric lumen, retards restitution in injured mucosae.
authors.affiliation: Department of Gastroenterology, Institute of Clinical Medicine, University of Tsukuba, Ibaraki 305-8575, Japan.
authors.forename: H
authors.initials: H
authors.lastname: Suzuki
authors.forename: A
authors.initials: A
authors.lastname: Yanaka
authors.forename: H
authors.initials: H
authors.lastname: Muto
mesh_terms: D000641:Ammonia / Q000378:metabolism*; D000643:Ammonium Chloride / Q000494:pharmacology; D000818:Animals; D017609:Barium Compounds / Q000494:pharmacology; D001692:Biological Transport / Q000187:drug effects; D002352:Carrier Proteins / Q000378:metabolism; D002412:Cations / Q000378:metabolism; D016764:Cell Polarity / Q000502:physiology; D002478:Cells, Cultured; D002712:Chlorides / Q000494:pharmacology; D015194:Diffusion Chambers, Culture; D004305:Dose-Response Relationship, Drug; D004594:Electrophysiology; D004847:Epithelial Cells / Q000166:cytology / Q000378:metabolism; D005260:Female; D005753:Gastric Mucosa / Q000166:cytology / Q000378:metabolism* / Q000382:microbiology; D006168:Guinea Pigs; D016481:Helicobacter Infections / Q000378:metabolism / Q000473:pathology; D016480:Helicobacter pylori; D008353:Mannitol / Q000493:pharmacokinetics; D008564:Membrane Potentials / Q000187:drug effects; D017830:Octoxynol / Q000633:toxicity; D015221:Potassium Channels / Q000378:metabolism; D012965:Sodium Chloride / Q000494:pharmacology; D028021:Sodium-Potassium-Chloride Symporters; D013276:Stomach Ulcer / Q000378:metabolism* / Q000382:microbiology / Q000473:pathology; D013501:Surface-Active Agents / Q000633:toxicity; D014316:Tritium; D014617:Vacuoles / Q000473:pathology
chemical_list: D017609:Barium Compounds; D002352:Carrier Proteins; D002412:Cations; D002712:Chlorides; D015221:Potassium Channels; D028021:Sodium-Potassium-Chloride Symporters; D013501:Surface-Active Agents; D000643:Ammonium Chloride; C024986:barium chloride; D014316:Tritium; D008353:Mannitol; D012965:Sodium Chloride; D000641:Ammonia; D017830:Octoxynol