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The Cellular Mechanisms of Tumor Necrosis Factor-Induced Mortality: A Possible Role for Platelet Activating Factor and/or the Eicosanoids

  • J. M. Moore
  • M. Hubbard
  • M. Earnest
  • P. Williams
  • A. DiSimone
  • N. Abumrad
  • J. R. Fletcher

Abstract

Tumor necrosis factor (TNF) is hailed as the seminal mediator in endotoxemia and/or sepsis in animals and humans [1, 2]. Of particular interest recently has been the reported role of eicosanoids (PGS) and platelet activating factor (PAF) in mediating many of the events in the pathophysiology of endotoxemia/sepsis in animals [3, 4]. Interestingly, the putative effects of PAF and the eicosanoids alone or in endotoxemia/sepsis are very similar to those attributed to TNF. To make the situation even more complex, TNF stimulates endothelial cells or fibroblasts to synthesize PAF [5], prostacyclin [6], or PGE2 [7] as well as many other potent cellular effectors.

Keywords

Tumor Necrosis Factor Metabolic Acidosis Platelet Activate Factor Cyclooxygenase Inhibitor Histological Abnormality 
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

© Springer-Verlag, Berlin Heidelberg 1993

Authors and Affiliations

  • J. M. Moore
    • 1
  • M. Hubbard
    • 1
  • M. Earnest
    • 1
  • P. Williams
    • 1
  • A. DiSimone
    • 1
  • N. Abumrad
    • 1
  • J. R. Fletcher
    • 2
  1. 1.Vanderbilt UniversityNashvilleUSA
  2. 2.Department of SurgeryUniversity of South AlabamaMobileUSA

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