Background:Helicobacter pylori(Hp) infection is involved in various gastroduodenal pathologies. Also, the potential role of Hp infection has been proposed in several extragastroduodenal disorders, such as cardiovascular, skin or immunological diseases. The role of Hp infection in acute pancreatitis has not been tested. The aim of this study was to determine the influence of Hp infection on the course of acute ischemia/reperfusion-induced pancreatitis in rats. Methods: Inoculation with CagA- and VacA-positive Hp or administration of vehicle were performed after visceral ischemia. Visceral ischemia was evoked by clamping of the celiac artery for 30 min. Four weeks later, after full recovery from primary ischemia-induced damage, acute pancreatitis was evoked by limitation of pancreatic blood flow (PBF) in the splenic artery for 30 min using microvascular clips. Rats were sacrificed 1 h or 1, 3, 5, 10, and 21 days after removal of the vascular clips. Hp infection was assessed by the urease test and gastric histology. Results: In Hp- negative rats ischemia followed by reperfusion caused acute pancreatitis as manifested by a reduction in PBF and pancreatic DNA synthesis, as well as by increases in plasma amylase, lipase, interleukin-1β (IL-1β) and interleukin-10 (IL-10). The morphological features of pancreatic tissue showed necrosis, strongly pronounced edema, hemorrhages and leukocyte infiltration. The maximal intensity of pancreatic damage was observed between the 1st and 3rd day of reperfusion, then pancreatic tissue underwent regeneration. Hp infection resulted in a significant reduction in PBF and an aggravation of pancreatic ischemia 1 h and 3 and 5 days after reperfusion. Plasma amylase in Hp- infected rats was significantly higher than in Hp- negative animals 1 h and 1 and 3 days after ischemia, whereas in lipase this significant difference was observed between the 1st and 3rd day. DNA synthesis in Hp-positive rats was additionally reduced 1 h and 3 and 5 days after ischemia. Also ischemia evoked an increase in serum IL-1β and IL-10, and morphological manifestations of pancreatitis were additionally enhanced by Hp infection. Conclusions: (1) Hp infection increases the severity of ischemia-induced pancreatitis; (2) Hp infection increases production of pro-inflammatory IL-1β, and (3) Hp infection aggravates disturbances in pancreatic microcirculation in acute pancreatitis.

Keywords:
Helicobacter pylori, Acute pancreatitis, Pancreatic blood flow, Interleukin-1β
This content is only available via PDF.
© 2002 S. Karger AG, Basel and IAP
2002
Copyright / Drug Dosage / Disclaimer
Copyright: All rights reserved. No part of this publication may be translated into other languages, reproduced or utilized in any form or by any means, electronic or mechanical, including photocopying, recording, microcopying, or by any information storage and retrieval system, without permission in writing from the publisher.
Drug Dosage: The authors and the publisher have exerted every effort to ensure that drug selection and dosage set forth in this text are in accord with current recommendations and practice at the time of publication. However, in view of ongoing research, changes in government regulations, and the constant flow of information relating to drug therapy and drug reactions, the reader is urged to check the package insert for each drug for any changes in indications and dosage and for added warnings and precautions. This is particularly important when the recommended agent is a new and/or infrequently employed drug.
Disclaimer: The statements, opinions and data contained in this publication are solely those of the individual authors and contributors and not of the publishers and the editor(s). The appearance of advertisements or/and product references in the publication is not a warranty, endorsement, or approval of the products or services advertised or of their effectiveness, quality or safety. The publisher and the editor(s) disclaim responsibility for any injury to persons or property resulting from any ideas, methods, instructions or products referred to in the content or advertisements.
You do not currently have access to this content.