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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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