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      Effect of Hyperosmolality upon the Mesothelial Monolayer Exposed in vivo and in situ to a Mannitol-Enriched Dialysis Solution

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          Abstract

          Studies done using the in vivo mouse model of population analysis of mesothelium showed that dialysis solutions containing high concentrations of glucose induced the development of a hypertrophic phenotype. Since these changes were neither related to the low pH nor to the presence of lactate buffer, we hypothesized that the presence of glucose was at the origin of the observed alterations. Theoretical analysis of the problem points to three possible mechanisms: hyperosmolality; metabolic changes derived from the high-glucose concentration itself, and/or the presence of products derived from the nonenzymatic degradation of glucose. The present study was designed to demonstrate or rule out the eventual effect of hyperosmolality upon the monolayer, applying the in vivo mouse model of population analysis of mesothelium. For this purpose, morphometric observations made in mice injected once a day during 30 consecutive days with a filter-sterilized 4.25% solution of mannitol (233.29 mM) were compared with those seen in intact mice and in a previously reported group of animals exposed to heat-sterilized fluid, having an equimolar concentration of glucose (235.9 mM), and the same osmolality (486 mosm/l) and electrolyte concentrations. The main findings observed in the mannitol-treated mice during the period of exposure included increased cell size and cytoplasmic surface area, as well as decreased cell viability. The regenerative capabilities of the exposed mesothelium remained intact. After a recovery period of 7 days, the aforementioned parameters reverted to normal values. This pattern is significantly different from the hypertrophic, senescent and low regenerative phenotype observed in mice treated with the high-glucose concentration solution. We conclude that, at least in the in vivo and in situ setup, the detrimental effects of hyperosmolality alone upon the exposed mesothelium are quite limited and fully reversible within a recovery period of 7 days.

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          ORE, a Eukaryotic Minimal Essential Osmotic Response Element

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            Biocompatibility of a Glucose-Free, Acidic Lactated Solution for Peritoneal Dialysis Evaluated by Population Analysis of Mesothelium

            Glucose-enriched, racemic lactate buffered solutions for peritoneal dialysis induce a significant reduction of cell viability as well as a hypertrophic, senescent phenotype of the exposed monolayer. The present study was designed to verify whether the aforementioned changes resulted form the buffer, from the osmotic agent, or from a combined effect of both. Mice were acutely (2 h) and long-term (15 and 30 days) exposed to daily intraperitoneal injections of a racemic lactate, heat-sterilized, low-pH (5.2), glucose-free solution. Imprints of the monolayer were taken at the end of each time interval. The glucose-free lactated buffer used in the present study did not induce significant changes in density distribution, mean cell size, mean cytoplasmic surface area, prevalence of large cells, multinucleation, proportion of observed cells in mitosis, and cell viability. So far, the previously mentioned hypertrophic phenotype appears to derive from substantial alterations in the cell cycle of mesothelium exposed to high concentrations of glucose and/or advanced glycosylation end products and unrelated to lactate.
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              Author and article information

              Journal
              NEF
              Nephron
              10.1159/issn.1660-8151
              Nephron
              S. Karger AG
              1660-8151
              2235-3186
              1999
              March 1999
              26 February 1999
              : 81
              : 3
              : 301-309
              Affiliations
              Department of Nephrology and Hypertension and Kornach Laboratory for Experimental Nephrology, ‘Ha′Emek’ Medical Center, Afula, Israel
              Article
              45297 Nephron 1999;81:301–309
              10.1159/000045297
              10050085
              © 1999 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: 7, Tables: 1, References: 36, Pages: 9
              Product
              Self URI (application/pdf): https://www.karger.com/Article/Pdf/45297
              Categories
              Original Paper

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