Tempel G E, Strong J W, Wise W C, Cook J A, Smith E F, Halushka P V
Dept of Physiology, Medical University of South Carolina, Charleston 29425.
Prog Clin Biol Res. 1989;299:33-42.
The vasoactive metabolites of arachidonic acid TxA2 and sulfidopeptide-leukotrienes appear to play a role in mediating hemodynamic alterations in endotoxic shock. The ultimate goal of these and other studies in shock is, however, to understand the mechanisms underlying the pathogenic changes in human shock states in order to develop effective treatment. Recent studies (see reviews by Ball, 1988) have implicated eicosanoids in pathogenesis of shock in man confirming the directions provided by the bolus endotoxin studies and suggest additional investigations of hemodynamics following interventions designed to alter eicosanoid synthesis in shock.
