RT Journal Article SR Electronic T1 Studies on the gastric mucosal microcirculation. 2.Helicobacter pylori water soluble extracts induce platelet aggregation in the gastric mucosal microcirculation in vivo JF Gut JO Gut FD BMJ Publishing Group Ltd and British Society of Gastroenterology SP 748 OP 752 DO 10.1136/gut.41.6.748 VO 41 IS 6 A1 N Kalia A1 S Jacob A1 N J Brown A1 M W R Reed A1 D Morton A1 K D Bardhan YR 1997 UL http://gut.bmj.com/content/41/6/748.abstract AB Background—The exact mechanisms by whichHelicobacter 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 microscopy assessed macromolecular leakage of labelled albumin from mucosal vessels, leucocyte adherence/rolling, and platelet activity for 90 minutes. Results—H pylori induced increases (p<0.001) in adherent platelet thrombi and circulating platelet emboli after five and 15 minutes respectively. Adherent platelet thrombi (mean of four per field of view) remained significantly increased throughout the experiment, but circulating emboli (maximum of five at 30 minutes) decreased with time. Leucocyte adherence did not occur although early transient rolling was observed. An 11% increase (p<0.02) in albumin leakage occurred after five minutes only. The induction of platelet aggregation was only observed following H pyloriadministration. Conclusion—This in vivo study demonstrated the ability of H pylori extracts to promote platelet aggregation 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 subsequent leucocyte recruitment by activated platelets.