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PAF and TNFα Interactions in the Pathophysiology of Septic Shock

  • Reuven Rabinovici
  • Tian Li Yue
  • Jerome Vernick
  • Giora Feuerstein
Part of the Advances in Experimental Medicine and Biology book series (AEMB, volume 314)

Abstract

The septic shock syndrome is a medical emergency caused in part by the release into the circulation of bacterial lipopolysaccharide (LPS) endotoxin. The evolving concept in the pathophysiology of septic shock suggests that endotoxin induces its detrimental effects indirectly through the production of multiple mediators among which platelet activating factor (PAF) and tumor necrosis factor-a (TNFa) play a major role. The role of PAF and TNFa in endotoxemia was inferred from the following observations: 1 ) many of the manifestations of septic shock such as hypotension, hemoconcentration, thrombocytopenia and leukopenia can be produced by PAF and TNFa (Table 1 ); 2) elevated levels of PAF and TNFa were found in various septic conditions (Table 2); and 3) PAF antagonists and anti-TNFa neutralizing antibodies were shown to convey significant protection in animal models of septic shock (Table 3).

Keywords

Septic Shock Disseminate Intravascular Coagulation Lipid Mediator Endotoxic Shock Produce Oxygen Radical 
These keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.

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Copyright information

© Plenum Press, New York 1991

Authors and Affiliations

  • Reuven Rabinovici
    • 2
  • Tian Li Yue
    • 1
  • Jerome Vernick
    • 2
  • Giora Feuerstein
    • 1
  1. 1.Department of Cardiovascular PharmacologySmithKline Beecham PharmaceuticalsKing of PrussiaUSA
  2. 2.Department of SurgeryJefferson Medical CollegePhiladelphiaUSA

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