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Complement and Endotoxin in Lung Injury

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Acute Lung Injury

Part of the book series: Update in Intensive Care and Emergency Medicine ((UICM,volume 30))

Abstract

The acute respiratory distress syndrome (ARDS) is characterized by progressive hypoxemia, decreased pulmonary compliance, and roentgenographic evidence of diffuse pulmonary infiltrates. The mechanisms that initiate, and then perpetuate the lung inflammation seen in ARDS remain poorly understood. Initially the syndrome was thought to involve only the lungs and to be the result of a single process; activation of the complement cascade. Subsequent investigations have shown that the injury is neither limited to the lungs nor is the pathogenesis simple. Neutrophil sequestration and migration within the lung remain histologic hallmarks of ARDS. It is likely that neutrophil recruitment and subsequent retention are the result of both chemotactic stimuli released within the lungs and activation of neutrophils by circulating mediators. Both complement components and lipopolysaccharide (LPS), a major component of the outer membrane of Gram-negative bacteria, have been implicated as important agents in the induction of ARDS.

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Authors
  1. K. E. Greene
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  2. P. E. Parsons
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Editors and Affiliations

  1. Pulmonary and Critical Care, St. Paul Ramsey Medical Center, 640 Jackson Street, St. Paul, 55101, MN, USA

    John J. Marini

  2. Anaesthesia and Critical Care, Royal Brompton Hospital, Sydney Street, SW3 6NP, London, UK

    Timothy W. Evans

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© 1998 Springer-Verlag Berlin Heidelberg

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Greene, K.E., Parsons, P.E. (1998). Complement and Endotoxin in Lung Injury. In: Marini, J.J., Evans, T.W. (eds) Acute Lung Injury. Update in Intensive Care and Emergency Medicine, vol 30. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-642-60733-2_4

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  • DOI: https://doi.org/10.1007/978-3-642-60733-2_4

  • Publisher Name: Springer, Berlin, Heidelberg

  • Print ISBN: 978-3-642-64532-7

  • Online ISBN: 978-3-642-60733-2

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