Abstract The fact that PAF-acether elicites acute circulatory collapse in anesthetized dogs supports the hypothesis that its endogenous double is involved in shock state events. The fact that cysteinyl containing leukotrienes has been shown to be released in various shock states, themselves producing noxious effects related to such circulatory disturbances, suggests a possible role of these arachidonic acid metabolites in shock syndrome. The present report summarizes the part played by these mediators in shock developments. More precisely, nanograms PAF-acether IV in anesthetized dogs produced biphasic effects on mesenteric blood flow and inhibited, in dogs and rats, histamine induced gastric acid secretion. These results confirm the distributive component of the PAF-acether circulatory collapse. On the other hand, as leukotrienes, nanograms PAF-acether elicited both plasma extravasation and vasoconstriction in guinea pig skin. Lastly, in conscious mice, lipoxygenase antagonists, but not cyclooxygenase antagonists, inhibited lethal effects of PAF-acether, suggesting a mutual and synergistic action of PAF-acether and leukotrienes in shock state.