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Cellular Metabolism in Sepsis

  • Chapter
Tissue Oxygen Utilization

Part of the book series: Update in Intensive Care and Emergency Medicine ((UICM,volume 12))

Abstract

The mechanism, or mechanisms, of cellular dysfunction during septic shock are not well understood. These mechanisms may include decreases in peripheral O2 transport, defective tissue O2 extraction, venous pooling of blood, extravasation of fluid into the interstitium, micro-circulatory abnormalities produced by the release of vasoactive mediators resulting in a regional mismatch of perfusion to cellular O2 requirements, the action of oxygen free radical species, the inhibitory effect on cardiac function of a myocardial depressant substance, and the direct noxious cellular effect of endotoxin or a mediator of sepsis [1–8].

Supported in part by a grant from the National Institutes of Health (HL41415-01).

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Authors
  1. G. Gutierrez
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  2. A. Dubin
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Editor information

Editors and Affiliations

  1. Pulmonary Medicine, Health Science Center, 6431 Fannin, Suite 1274, 77030, Houston, TX, USA

    Guillermo Gutierrez

  2. Department of Intensive Care, Erasme University Hospital, Free University of Brussels, Route de Lennik 808, 1070, Brussels, Belgium

    Jean Louis Vincent (Clinical Director) (Clinical Director)

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© 1991 Springer-Verlag Berlin Heidelberg

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Gutierrez, G., Dubin, A. (1991). Cellular Metabolism in Sepsis. In: Gutierrez, G., Vincent, J.L. (eds) Tissue Oxygen Utilization. Update in Intensive Care and Emergency Medicine, vol 12. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-642-84169-9_18

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  • DOI: https://doi.org/10.1007/978-3-642-84169-9_18

  • Publisher Name: Springer, Berlin, Heidelberg

  • Print ISBN: 978-3-540-52472-4

  • Online ISBN: 978-3-642-84169-9

  • eBook Packages: Springer Book Archive

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