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

A A Mathé; K Strandberg; S S Yen

doi:10.1016/0090-6980(77)90288-x

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

A A Mathé·K Strandberg·S S Yen

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Abstract

Slow reacting substance (SRS) injected into the pulmonary artery released prostaglandins E (PGE) and F2alpha (PGF2alpha) 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, PGF2alpha and the metabolites when incubated with SRS or antigen. In in vivo experiments, SRS and arachidonic acid given intravenously increased the airway insufflation pressure in anesthetized quinea pigs. These effects, but not the action of injected PGF2alpha 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.

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Airway Resistance Animals Antigen-Antibody Reactions Arachidonic Acids Autacoids Guinea Pigs Histamine Humans Indomethacin Injections, Intra-Arterial Lung Prostaglandins E Prostaglandins F Pulmonary Artery Journal Article Research Support, U.S. Gov't, P.H.S.

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A A Mathé, K Strandberg, S S Yen. 1977. Prostaglandin release by slow reacting substance from guinea pig and human lung tissue.. https://doi.org/10.1016/0090-6980(77)90288-x

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