Prostaglandin release by slow reacting substance from guinea pig and human lung tissue

Slow reacting substance (SRS) injected into the pulmonary artery released prostaglandin E (PGE) and F_2α (PGF_2α) and the 15-keto-13, 14-dihydro PG metabolites from non-sensitized and ovalbumin sensitized, isolated, perfused guinea pig lungs. PGs were also released from lungs incubated with SRS. Sensitized lungs released more PGs in both types of preparations. Indomethacin inhibited the effect of SRS. Passively sensitized human lung fragments, in parallel to guinea pig lung, released PGE, PGF_2α and the metabolites when incubatted with SRS or antigen. In experiments, SRS and arachidonic acid given intravenously increased the airway insufflation pressure in anesthetized guinea pigs. These effects, but not the action of injected PGF_2α and histamine, were abolished by indomethacin. The results indicate that one of the modes of SRS action is by release of PGs, and are consistent with the hypothesis that PGs are predominantly “secondary” mediators (in the temporal sense) of the antigen-antibody reaction.