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Microvascular Regulation of Tissue Oxygenation in Sepsis

  • Conference paper
Yearbook of Intensive Care and Emergency Medicine 1998

Part of the book series: Yearbook of Intensive Care and Emergency Medicine ((YEARBOOK,volume 1998))

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Abstract

Sepsis and its related syndromes develop frequently in hospitalized patients, with an associated mortality of 10–20%. In the presence of circulatory failure, this figure rises to over 60% and may account for up to 200,000 deaths per annum in the USA alone [1]. Most patients succumb to a multiple organ dysfunction syndrome (MODS) rather than hypotension per se [2], but the reasons for this are not clear. Sepsis is known to disrupt microcirculatory flow and nutrient exchange, and an impaired response to endogenous and exogenous pressor agents is often reported [3]. Intravascular leukaggregation, abnormal red blood cell deformability, increased microvascular permeability, interstitial protein loss and tissue edema are frequently observed [4]. This systemic inflammatory response is promoted not only by reduced perfusion of nutrient vessels, but also from pro-inflammatory mediators released from activated, sequestered leukocytes, and activated macrophages, platelets and endothelial cells. It has been hypothesized that endothelial injury exacerbates maldistribution of regional blood flow leading to cellular hypoxia and vital organ dysfunction. Various injurious substances as well as several microbacteria toxins (e.g., peptoglycans from Gram-positive bacteria) may initiate this response. However, the most severe septic microvascular inflammatory responses are observed with Gram-negative bacteria, or more specifically the cell wall component, endotoxin.

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© 1998 Springer-Verlag Berlin Heidelberg

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Anning, P.B., Sair, M., Evans, T.W. (1998). Microvascular Regulation of Tissue Oxygenation in Sepsis. In: Vincent, JL. (eds) Yearbook of Intensive Care and Emergency Medicine 1998. Yearbook of Intensive Care and Emergency Medicine, vol 1998. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-642-72038-3_14

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  • DOI: https://doi.org/10.1007/978-3-642-72038-3_14

  • Publisher Name: Springer, Berlin, Heidelberg

  • Print ISBN: 978-3-540-63798-1

  • Online ISBN: 978-3-642-72038-3

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