STUDIES ON THE GASTRIC-MUCOSAL MICROCIRCULATION - 2 - HELICOBACTER-PYLORI WATER-SOLUBLE EXTRACTS INDUCE PLATELET-AGGREGATION IN THE GASTRIC-MUCOSAL MICROCIRCULATION IN-VIVO

Background-The exact mechanisms by which Helicobacter pylori infection results in gastric mucosal injury are unclear. Aims-To assess in vivo whether H pylori extracts could initiate an inflammatory response in the rat gastric mucosal microcirculation. Methods-Extracts of H pylori , Escherichia coli, or distilled water were administered topically to the gastric mucosa of anaesthetised animals. Fluorescence in vivo micr oscopy assessed macromolecular leakage of labelled albumin from mucosa l vessels, leucocyte adherence/rolling, and platelet activity for 90 m inutes. Results-H pylori induced increases (p<0.001) in adherent plate let thrombi and circulating platelet emboli after five and 15 minutes respectively. Adherent platelet thrombi (mean of four per field of vie w) remained significantly increased throughout the experiment, but cir culating emboli (maximum of five at 30 minutes) decreased with time. L eucocyte adherence did not occur although early transient rolling was observed. An 11% increase (p<0.02) in albumin leakage occurred after f ive minutes only. The induction of platelet aggregation was only obser ved following H pylori administration. Conclusion-This in vivo study d emonstrated the ability of H pylori extracts to promote platelet aggre gation within gastric mucosal microvessels. Recruitment of leucocytes was not observed. The results suggest that the early events associated with H pylori infection are platelet aggregation with perhaps subsequ ent leucocyte recruitment by activated platelets.