Effects of chronic administration of Helicobacter pylori extracts on rat gastric mucosal microcirculation in vivo

The mechanisms by which Helicobacter pylori contributes to gastroduodenal injury are unclear, We have previously described platelet aggregation within rat gastric mucosal microcirculation following acute administration of H. pylori extracts. However, leukocyte activation was not observed. This study aimed to determine whether chronic administration of H. pylori could induce leukocyte activation. Rats were gavaged with either H. pylori or E. coli extracts or with distilled water three times daily at three-day intervals. Acridine red was used to quantitate gastric mucosal leukocyte/platelet activity using fluorescent in vivo microscopy. Further animals received additional acute H. pylori after 1 hr and recordings were made for a further 1 hr. Significant numbers of "flyers," "rollers," and adherent leukocytes were observed throughout the study in H. pylori animals. Only adherent leukocytes were observed following E, coli. Acute H. pylori induced a further significant increase in adherent leukocytes. Significant platelet thrombi were also present in H. pylori-treated animals. In conclusion, earlier studies demonstrated platelet aggregation but no leukocyte activation, which is in contrast to the current chronic studies. Platelet activation may be the initial response to H. pylori and involved in recruitment of leukocytes. These activated cells may contribute to the development of gastric mucosal damage.