Putative effect of Helicobacter pylori and gastritis on gastric acid secretion in cat.
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.
Sobhani
Iradj
I
INSERM Unité 410, Hôpital Bichat Claude Bernard, 75877 Cedex Paris 18, France. iradj.sobhani@bch.ap-hop-paris.fr
Canedo
Sergio
S
Alchepo
Beatriz
B
Vissuzaine
Christiane
C
Chevalier
Catherine
C
Buyse
Marion
M
Moizo
Laurent
L
Laigneau
J Pierre
JP
Mignon
Michel
M
Lewin
J Miguel
JM
Bado
André
A
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
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