Studies on the gastric mucosal microcirculation. 2. Helicobacter pylori water soluble extracts induce plateletaggregation in the gastric mucosal microcirculation in vivo

摘要

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 microscopy assessed macromolecular leakage of labelled albumin from mucosal vessels, leucocyte adherence/rolling, and platelet activity for 90minutes.
Results—H pylori induced increases (p<0.001) in adherent platelet thrombi and circulating platelet emboli after five and 15minutes respectively. Adherent platelet thrombi (mean of four per field of view) remained significantly increased throughout the experiment, but circulating emboli (maximum of five at 30minutes) 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 pylori administration.
Conclusion—This in vivo study demonstrated theability of H pylori extracts to promoteplatelet aggregation within gastric mucosal microvessels. Recruitmentof leucocytes was not observed. The results suggest that the earlyevents associated with H pylori infection are plateletaggregation with perhaps subsequent leucocyte recruitment by activated platelets.

Keywords:gastric mucosal microcirculation; Helicobacterpylori; fluorescence in vivo microscopy; platelet aggregation; leucocytes