Nephron
Original Paper
Development of Renal Failure in Endotoxemic Rats: Can It Be Explained by Early Changes in Renal Energy Metabolism?van Lambalgen A.A.a · van Kraats A.A.a · van den Bos G.C.a · Teerlink T.b · Stel H.V.c · Donker A.J.M.d · Thijs L.G.daLaboratory for Physiology, bCentral Chemical Laboratory, and Departments of cPathology and dInternal Medicine, Free University, Amsterdam, The Netherlands
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Article / Publication Details
Accepted: October 23, 1992
Published online: December 12, 2008
Issue release date: 1993
Number of Print Pages: 7
Number of Figures: 0
Number of Tables: 0
ISSN: 1660-8151 (Print)
eISSN: 2235-3186 (Online)
For additional information: https://www.karger.com/NEF
Abstract
Endotoxin shock not only causes renal failure, endotoxemia also leads to metabolic impairment, resulting in energy shortage and loss of cellular integrity; therefore, we tested the hypothesis that early changes in renal metabolism contribute to the development of acute renal failure during endotoxin shock. Endotoxin (Escherichia coli127B8; 8 mg/kg from t = 0 to 60 min) was infused in three groups of 8 rats, in which renal biopsies were taken at t = 30,50 and 90 min, respectively; a fourth group (n – 8) served as control. In the biopsies, glucose, lactate, ATP, ADP, AMP and creatine phosphate concentrations were determined. Renal plasma flow (RPF) and glomerular filtration rate (GFR) were measured from the clearances of 131I-hippurate and 125I-thalamate, respectively. We also assayed urine flow (V; catheter in the bladder), cardiac output (CO), blood pressure (MAP), heart rate (HR) and arterial lactate, glucose and creatinine concentrations. During the first 30 min of endotoxemia, we found no systemic hemodynamic or biochemical changes. From t = 30 to t = 90, CO and MAP decreased to 59 and 70%, respectively, while HR and serum levels rose to 110 and 800%, respectively (p < 0.05), indicating progression of shock. Renal function clearly deteriorated from t = 30: at t = 90 RPF, GFR and V had decreased by 86, 84 and 86%, respectively, plasma creatinine being 193% of the baseline value (p < 0.05). In the t = 30 biopsies, the only change was an increase in glucose concentration (by 21% vs. control value; p < 0.05), which peaked at t = 50 (by 63%; p < 0.05), and was still elevated at t = 90 (by 43%; p < 0.05). The rise in renal lactate concentration paralleled that in serum lactate. There were, however, no differences in energy-rich phosphates between the four groups. Thus, our results show that endotoxemia causes early changes in RPF, GFR, V and renal glucose metabolism, but no early decrease in energy status.
© 1993 S. Karger AG, Basel
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Article / Publication Details
Accepted: October 23, 1992
Published online: December 12, 2008
Issue release date: 1993
Number of Print Pages: 7
Number of Figures: 0
Number of Tables: 0
ISSN: 1660-8151 (Print)
eISSN: 2235-3186 (Online)
For additional information: https://www.karger.com/NEF
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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.
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