GASTRIN-RELEASE AND GASTRIC-ACID SECRETION IN THE RAT INFECTED WITH EITHER HELICOBACTER-FELIS OR HELICOBACTER-HEILMANNII

Helicobacter pylori infection in humans has been shown to be associate d with changes in gastric physiology, including exaggerated basal and meal-stimulated gastrin levels. This has been suggested to be due to t he direct effects of the bacterium through inflammation and its urease enzyme. The gastric bacteria Helicobacter felis and Helicobacter heil mannii colonize the antrum of rats in large numbers and induce no sign ificant inflammatory response. Thus, the direct effect of Helicobacter infection on gastric physiology, independent of gastritis, could be s tudied. Basal, freely fed and stimulated acid and gastrin levels were recorded from animals infected with H. felis, H. heilmannii or uninfec ted controls over a 30 week period. No significant difference was foun d between freely fed gastrin over 7 weeks or fasting gastrin over 24 w eeks or basal and stimulated acid over 30 weeks between all three grou ps. Triple therapy did not alter gastrin or acid output. The antrum of all Helicobacter-infected rats was well colonized; triple therapy cle ared H. felis but not H. heilmannii. Very little inflammation was seen in control or Helicobacter-infected animals. In conclusion, Helicobac ter-induced effects on gastric physiology are unlikely to be due to di rect bacterial effects, but are best explained by other factors (i.e. inflammatory damage).