+1 Recommend
1 collections
      • Record: found
      • Abstract: found
      • Article: found

      Intraperitoneal Nitric Oxide Production in Patients Treated by Continuous Ambulatory Peritoneal Dialysis

      Read this article at

          There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.


          Background: Nitric oxide (NO) generation within the peritoneum could potentially affect peritoneal transport by increasing capillary vasodilatation, and increase peritoneal permeability during episodes of bacterial peritonitis. As peritoneal mesothelial cells have a common embryological derivation with endothelial cells, then mesothelial cells could potentially be a major source of locally produced NO. Methods: NO was measured using the Griess reaction in fresh and spent dialysate effluent (SPDE) from uninfected CAPD patients, and from those during episodes of bacterial peritonitis. Human peritoneal mesothelial cells (HPMC) were cultured and NO production determined in the presence of SPDE and the effect of a potential NO substrate, L-arginine, and NO synthase inhibitor, L-NMMA. NO production by peritoneal macrophages (MØ), obtained from SPDE and the effect of staphylococci was also determined. RNA for inducible nitric oxide synthase (iNOS) was sought using Northern blotting technique following combination stimulation with lipopolysaccharide and cytokines (IL-1β, TNF-α and γ-INF, and/or spent dialysate from patients with bacterial peritonitis). Results: Whereas fresh CAPD dialysate was nitrite-free, SPDE from the day time exchange contained 41 ± 3 µ M (nitrite and nitrate), and that from the overnight dwell 91 ± 8 µ M. During CAPD peritonitis, dialysate nitrite and nitrate increased from 9.3 ±0.8 to 17.5 ± 2.4 µ M/l·h, for the first CAPD bag at presentation, and 15.2 ± 1.8 for the second and 16.2 ± 2.4 for the third exchange (p < 0.01 compared to non-infected control). By the second day, levels had returned to baseline, 7.3 ± 0.9 µ M/l·h. HPMC produced 261 nmol nitrate and nitrite/mg cell protein, and this increased in a dose-dependent manner with the addition of spent uninfected CAPD dialysate, to 365 nmol/mg with 1:10 dilution and 655 nmol/mg with 1:2 dilution, p < 0.001. The addition of the substrate, L-arginine, resulted in a 10% increase in nitrite and nitrate production, whereas the addition of L-NMMA produced a 10% reduction. Peritoneal MØ obtained from SPDE produced similar quantities of nitrite and nitrate to peritoneal mesothelial cells, and cultures of Staphylococcus aureus resulted in a reduction in nitrite and nitrate levels, as they were used as a growth requirement. However, we could not demonstrate RNA production for iNOS by HPMC following cytokine or SPDE stimulation. Conclusions: This suggests that HPMC may be an important source of locally generated NO within the peritoneal cavity under basal conditions, but as they do not contain iNOS, the increased NO produced during episodes of acute bacterial peritonitis is more likely due to a combination of increased NO production by peritoneal endothelial cells and transmigrating macrophages.

          Related collections

          Most cited references 1

          • Record: found
          • Abstract: not found
          • Article: not found

          Experimental diabetes induces functional and structural changes in the peritoneum


            Author and article information

            Blood Purif
            Blood Purification
            S. Karger AG
            July 2004
            30 March 2004
            : 22
            : 2
            : 216-223
            Renal Research Laboratories, Centre for Nephrology, Royal Free Hospital, London, UK
            76856 Blood Purif 2004;22:216–223
            © 2004 S. Karger AG, Basel

            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.

            Page count
            Figures: 4, Tables: 2, References: 27, Pages: 8
            Self URI (application/pdf): https://www.karger.com/Article/Pdf/76856
            Original Paper


            Comment on this article