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Mitochondrial Metabolic Alterations in Experimental Circulatory Shock

  • Chapter
Gram-Negative Bacterial Infections and Mode of Endotoxin Actions

Abstract

Lethal endotoxemia induces hypoglycemia, high blood lactate/pyruvate ratios and decreased tissue oxygen utilization. All these metabolic symptoms occur simultaneously. This indicates that the cytoplasmic portion of cellular glucose metabolism, glycolysis, still must be operating, but the mitochondrial reactions, the tricarboxylic acid cycle and/or the electron transfer and oxidative phosphorylation reactions could have become defective. The fact that the gluconeogenetic pathway presumably is inhibited at three different points (5) could explain hypoglycemia and somewhat higher than normal lactate and pyruvate concentrations, but could not count for decreased oxygen utilization. Thus, it was important to us, as well as to some other investigators, to attempt a clarification of possible effects of endotoxemia on mitochondrial metabolic reactions. The importance of these studies is emphasized by the central role of adequate energy production in the survival of cells and vital tissue functions.

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Authors
  1. L. Mela
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Editors and Affiliations

  1. Abteilung für Immunologie und Serologie am Institut für Hygiene und Medizinische Mikrobiologie der Fakultät für Klinische Medizin Mannheim, Universität Heidelberg, Mannheim, Federal Republic of Germany

    Bernhard Urbaschek  & Renate Urbaschek  & 

  2. Departments of Microbiology and Pediatrics, State University of New York at Buffalo, Buffalo, N.Y., USA

    Erwin Neter M. D.

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© 1975 Springer-Verlag/Wien

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Mela, L. (1975). Mitochondrial Metabolic Alterations in Experimental Circulatory Shock. In: Urbaschek, B., Urbaschek, R., Neter, E. (eds) Gram-Negative Bacterial Infections and Mode of Endotoxin Actions. Springer, Vienna. https://doi.org/10.1007/978-3-7091-8396-0_36

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  • DOI: https://doi.org/10.1007/978-3-7091-8396-0_36

  • Publisher Name: Springer, Vienna

  • Print ISBN: 978-3-7091-8398-4

  • Online ISBN: 978-3-7091-8396-0

  • eBook Packages: Springer Book Archive

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