PENTAGASTRIN GASTROPROTECTION AGAINST ACID IS RELATED TO H-2-RECEPTORACTIVATION BUT NOT ACID-SECRETION

Background - Pentagastrin enhances gastric mucosal defence mechanisms against acid and protects the gastric mucosa from experimental injury. Aims - To investigate whether this gastroprotection is mediated by hi stamine receptors or occurs as a secondary effect of acid secretion st imulation. Methods - The effects of omeprazole (100 mu mol/kg), raniti dine (20 mg/kg), and pyrilamine (10 mg/kg) on pentagastrin (80 mu g/kg /h) induced gastroprotection against acidified aspirin injury were exa mined in a luminal pH controlled model. The effects of these compounds on pentagastrin enhanced gastroprotective mechanisms were investigate d using intravital microscopy, in which intracellular pH of gastric su rface cells (pH(i)), mucus gel thickness, gastric mucosal blood flow, and acid output were measured simultaneously. Results - Pentagastrin p rotected rat gastric mucosa from acidified aspirin injury. This gastro protection was abolished by ranitidine, but not omeprazole or pyrilami ne. Pentagastrin induced a hyperaemic response to luminal acid challen ge, increased mucus gel thickness, and elevated pH(i) during acid chal lenge. Ranitidine reversed these enhanced defence mechanisms, whereas omeprazole and pyrilamine preserved these effects. Conclusions - These data indicate that pentagastrin associated gastroprotection and enhan ced defence mechanisms against acid result mainly from activation of h istamine H-2 receptors, and not as an effect of the stimulation of aci d secretion.