Sobhani Iradj, Canedo Sergio, Alchepo Beatriz, Vissuzaine Christiane, Chevalier Catherine, Buyse Marion, Moizo Laurent, Laigneau J Pierre, Mignon Michel, Lewin J Miguel, Bado André
INSERM Unité 410, Hôpital Bichat Claude Bernard, 75877 Cedex Paris 18, France.
Am J Physiol Gastrointest Liver Physiol. 2002 Apr;282(4):G727-34. doi: 10.1152/ajpgi.00282.2001.
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.
幽门螺杆菌可能会增加或抑制胃酸分泌。我们以硫代酰胺（H₃受体拮抗剂）和SR - 27417A（血小板活化因子受体拮抗剂）为参照，研究了携带猫幽门螺杆菌、幽门螺杆菌或无胃部病原体的猫的胃酸变化和血浆胃泌素水平。在携带猫幽门螺杆菌的猫中，胃黏膜组织学检查正常。根除猫幽门螺杆菌后，与根除前相比，五肽胃泌素刺激的胃酸分泌增加了（40%）。硫代酰胺消除了猫幽门螺杆菌的这种抑制作用，而SR - 27417A则没有。基础和进餐刺激的血浆胃泌素水平不受根除治疗的影响。幽门螺杆菌感染后第3周胃酸分泌受到抑制（-80%），第5至9周增加，并在长达42周内保持稳定。SR - 27417A在第8周前对胃酸分泌没有影响，但此后会抑制胃酸分泌，而硫代酰胺仅在这些猫的第7周前使其增加（20%）。幽门螺杆菌通过H₃受体途径抑制胃酸分泌。因此，炎症介质参与了对幽门螺杆菌抑制胃酸分泌作用的适应性调节。
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