title: Gastric acid secretion in cyclooxygenase-1 deficient mice.
abstract: BACKGROUND
  Constitutive cyclooxygenase-1 enzyme synthesizes prostaglandins which are thought to play an important role in the functional integrity of the stomach gastric mucosa. Recently, it was shown that cyclooxygenase-1 deficient mutant mice did not develop spontaneous gastric pathology and appear less sensitive to indomethacin-induced gastric damage.
  
  
  OBJECTIVE
  To investigate gastric acid secretion in cyclooxygenase-1 deficient mutant mice.
  
  
  METHODS
  The basal and histamine or isobutyl methylxanthine-stimulated acid secretion in stomachs of cyclooxygenase-1 deficient homozygous mice and the effect of indomethacin was compared with that of heterozygous and wild-type mice using isolated lumen perfused mouse stomachs, in organ baths, monitored by pH-electrodes.
  
  
  RESULTS
  There was no significant difference in the basal or histamine stimulated gastric acid secretion between wild-type or heterozygous or homozygous mice. However, isobutyl methylxanthine was more potent in the cyclooxygenase-1 deficient and heterozygous mice than in wild-type mice. Indomethacin, at concentrations below 1 mM, had no effect on either basal or histamine stimulated acid secretion in any of the mice populations.
  
  
  CONCLUSIONS
  Gastric acid secretion is maintained without prostaglandin involvement in cyclooxygenase-1 deficient mice. The finding that basal and histamine-stimulated gastric acid secretion was similar in the cyclooxygenase-1 deficient, compared to wild-type mice is consistent with the lack of spontaneous gastric pathology in the cyclooxygenase-1 deficient mice.
authors.affiliation: Academic Department of Surgery, The Rayne Institute, GKT School of Medicine and Dentistry, King's College, London, UK.
authors.forename: F
authors.initials: F
authors.lastname: Borrelli
authors.forename: N J
authors.initials: NJ
authors.lastname: Welsh
authors.forename: G
authors.initials: G
authors.lastname: Sigthorsson
authors.forename: R
authors.initials: R
authors.lastname: Simpson
authors.forename: A
authors.initials: A
authors.lastname: Palizban
authors.forename: I
authors.initials: I
authors.lastname: Bjarnason
authors.forename: I A
authors.initials: IA
authors.lastname: Tavares
mesh_terms: D015056:1-Methyl-3-isobutylxanthine / Q000494:pharmacology; D000465:Algorithms; D000818:Animals; D051545:Cyclooxygenase 1; D016861:Cyclooxygenase Inhibitors / Q000633:toxicity; D005744:Gastric Acid / Q000378:metabolism*; D005838:Genotype; D006632:Histamine / Q000494:pharmacology; D006863:Hydrogen-Ion Concentration; D066298:In Vitro Techniques; D007213:Indomethacin / Q000633:toxicity; D007527:Isoenzymes / Q000172:deficiency* / Q000235:genetics; D008565:Membrane Proteins; D051379:Mice; D008810:Mice, Inbred C57BL; D018345:Mice, Knockout; D010477:Perfusion; D010726:Phosphodiesterase Inhibitors / Q000494:pharmacology; D011451:Prostaglandin-Endoperoxide Synthases / Q000172:deficiency* / Q000235:genetics; D011453:Prostaglandins / Q000378:metabolism
chemical_list: D016861:Cyclooxygenase Inhibitors; D007527:Isoenzymes; D008565:Membrane Proteins; D010726:Phosphodiesterase Inhibitors; D011453:Prostaglandins; D006632:Histamine; D051545:Cyclooxygenase 1; D011451:Prostaglandin-Endoperoxide Synthases; C496512:Ptgs1 protein, mouse; D015056:1-Methyl-3-isobutylxanthine; D007213:Indomethacin