title: Putative effect of Helicobacter pylori and gastritis on gastric acid secretion in cat.
abstract: Helicobacter pylori may increase or inhibit gastric acid. We studied acid variations and plasma gastrin in cats harboring Helicobacter felis, harboring H. pylori, or free of gastric pathogens with reference to thioperamide (H(3) receptor antagonist) and SR-27417A (PAF receptor antagonist). In cats harboring H. felis, gastric mucosa were histologically normal. After H. felis eradication, pentagastrin-stimulated acid secretion was increased (40%) compared with the situation before eradication. Thioperamide abolished this inhibitory effect of H. felis, whereas SR-27417A did not. Basal and meal-stimulated plasma gastrin levels were not affected by eradication therapy. Acid secretion was inhibited (-80%) in week 3, increased from weeks 5 to 9, and remained constant for up to 42 weeks after H. pylori infection. SR-27417A had no effect on acid secretion before week 8 but inhibited it thereafter, and thioperamide increased it (20%) only before week 7 in those cats. Helicobacter inhibits gastric acid via an H(3) receptor pathway. Inflammatory mediators are thus involved in adaptation to the inhibitory effects of H. pylori on acid secretion.
authors.affiliation: INSERM Unité 410, Hôpital Bichat Claude Bernard, 75877 Cedex Paris 18, France. iradj.sobhani@bch.ap-hop-paris.fr
authors.forename: Iradj
authors.initials: I
authors.lastname: Sobhani
authors.forename: Sergio
authors.initials: S
authors.lastname: Canedo
authors.forename: Beatriz
authors.initials: B
authors.lastname: Alchepo
authors.forename: Christiane
authors.initials: C
authors.lastname: Vissuzaine
authors.forename: Catherine
authors.initials: C
authors.lastname: Chevalier
authors.forename: Marion
authors.initials: M
authors.lastname: Buyse
authors.forename: Laurent
authors.initials: L
authors.lastname: Moizo
authors.forename: J Pierre
authors.initials: JP
authors.lastname: Laigneau
authors.forename: Michel
authors.initials: M
authors.lastname: Mignon
authors.forename: J Miguel
authors.initials: JM
authors.lastname: Lewin
authors.forename: André
authors.initials: A
authors.lastname: Bado
mesh_terms: D000818:Animals; D000900:Anti-Bacterial Agents / Q000627:therapeutic use; D002415:Cats; D005744:Gastric Acid / Q000378:metabolism*; D005753:Gastric Mucosa / Q000473:pathology; D005755:Gastrins / Q000097:blood; D005756:Gastritis / Q000382:microbiology* / Q000473:pathology / Q000503:physiopathology*; D016998:Helicobacter / Q000302:isolation & purification; D016481:Helicobacter Infections / Q000188:drug therapy / Q000503:physiopathology*; D016480:Helicobacter pylori / Q000302:isolation & purification / Q000502:physiology*; D006633:Histamine Antagonists / Q000494:pharmacology; D007700:Kinetics; D010418:Pentagastrin / Q000494:pharmacology; D010880:Piperidines / Q000494:pharmacology; D010980:Platelet Membrane Glycoproteins / Q000037:antagonists & inhibitors; D011956:Receptors, Cell Surface; D043562:Receptors, G-Protein-Coupled; D018100:Receptors, Histamine H3 / Q000187:drug effects; D013844:Thiazoles / Q000494:pharmacology; D014510:Urease / Q000032:analysis
chemical_list: D000900:Anti-Bacterial Agents; D005755:Gastrins; D006633:Histamine Antagonists; D010880:Piperidines; D010980:Platelet Membrane Glycoproteins; D011956:Receptors, Cell Surface; D043562:Receptors, G-Protein-Coupled; D018100:Receptors, Histamine H3; D013844:Thiazoles; C039351:platelet activating factor receptor; D014510:Urease; D010418:Pentagastrin; C052075:thioperamide; C071317:Foropafant