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Am J Physiol Gastrointest Liver Physiol 282: G727-G734, 2002. First published November 28, 2001; doi:10.1152/ajpgi.00282.2001
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Vol. 282, Issue 4, G727-G734, April 2002

Putative effect of Helicobacter pylori and gastritis on gastric acid secretion in cat

Iradj Sobhani1, Sergio Canedo1, Beatriz Alchepo1, Christiane Vissuzaine2, Catherine Chevalier3, Marion Buyse1, Laurent Moizo1, J. Pierre Laigneau1, Michel Mignon1, J. Miguel Lewin1, and André Bado1

1 INSERM Unité 410 and 2 Service d'Anatomie pathologique, Hôpital Bichat Claude Bernard, 75877 Cedex Paris 18; and 3 Laboratoire des entérobactéries, Institut Pasteur, 75015 Paris, France

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 (H3 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 H3 receptor pathway. Inflammatory mediators are thus involved in adaptation to the inhibitory effects of H. pylori on acid secretion.

histamine; gastrin; PAF receptor; H3 receptor




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