Leukotrienes in Endotoxin Shock

  • W. Hagmann
  • C. Denzlinger
  • S. Rapp
  • D. Keppler
Conference paper
Part of the NATO ASI Series book series (NSSA, volume 139)


Actions of endotoxin (1ipopolysaccharide, LPS) in vivo have long been suggested to be mediated by arachidonate metabolites (1,2). The important role of arachidonate-derived metabolites including leukotrienes, prostaglandins and thromboxane in experimental LPS shock has been deduced from the LPS resistance of essential fatty acid-deficient rats (3,4), from the altered arachidonate metabolism in LPS-tolerant rats (5), as well as from pharmacological evidence (1,2,6,7). Recent studies showed that the LPS-resistant C3H/HeJ mouse strain, whose macrophages are defective in prostaglandin (8,9) and leukotriene synthesis (10), can be made highly LPS-sensitive by transfer of pure macrophages from LPS-sensitive C3H/HeN mice (11). These data stress the target cell role of macrophages in the in vivo action of LPS (8,11).


Bile Duct Ligation Circ Shock Endotoxin Shock Pharmacological Evidence Lethal Action 
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Copyright information

© Plenum Press, New York 1987

Authors and Affiliations

  • W. Hagmann
    • 1
  • C. Denzlinger
    • 1
  • S. Rapp
    • 1
  • D. Keppler
    • 1
  1. 1.Biochemisches InstitutUniversity of FreiburgFreiburgWest Germany

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