Therapeutic options directed against platelet activating factor, eicosanoids and bradykinin in sepsis
Author(s) -
Marina Fink
Publication year - 1998
Publication title -
journal of antimicrobial chemotherapy
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.124
H-Index - 194
eISSN - 1460-2091
pISSN - 0305-7453
DOI - 10.1093/jac/41.suppl_1.81
Subject(s) - autacoid , bradykinin , platelet activating factor , sepsis , platelet , eicosanoid , medicine , thromboxane a2 , septic shock , receptor , thromboxanes , immunology , pathogenesis , pharmacology , thromboxane , biology , arachidonic acid , enzyme , biochemistry
Various autacoids, including the eicosanoids, platelet activating factor (PAF) and bradykinin, have been implicated in the pathogenesis of sepsis and septic shock. The precise role of these compounds as mediators of the diffuse inflammatory state characteristic of sepsis remains to be determined, but, in animal models, beneficial effects have been observed as a result of treatment with various inhibitors of eicosanoid biosynthesis or antagonists of PAF or bradykinin receptors. To date, however, it has been impossible to translate these encouraging results from animal models into convincingly positive results in the clinical setting.
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