Abstract
Fragments of chopped lung from indomethacin treated guinea-pigs had an anti-aggregating effect when added to human platelet rich plasma (PRP), probably due to the production of prostacyclin (PGI 2) since the effect was inhibited by 15-hydroperoxy arachidonic acid (15-HPAA, 10 μg ml −1). Both 15-HPAA (1–20 μg ml −1 min −1) and 13-hydroperoxy linoleic acid (13-HPLA, 20 μg ml −1 min −1) caused a marked enhancement of the anaphylactic release of histamine, slow-reacting substance of anaphylaxis (SRS-A) and rabbit aorta contracting substance (RCS) from guinea-pig isolated perfused lungs. This enhancement was not reversed by the concomitant infusion of either PGI 2 (5 μg ml −1 min −1) or 6-oxo-prostaglandin F 1α (6-oxo-PGF 1α, 5 μg ml −1 min −1). Anaphylactic release of histamine and SRS-A from guinea-pig perfused lungs was not inhibited by PGI 2 (10 ng - 10 μg ml −1 min −1) but was inhibited by PGE 2 (5 and 10 μg ml −1 min −1). Antiserum raised to 5,6-dihydro prostacyclin (PGI 1) in rabbits, which also binds PGI 2, had no effect on the release of anaphylactic mediators. The fatty acid hydroperoxides may enhance mediator release either indirectly by augmenting thromboxane production or by a direct effect on sensitized cells. Further experiments to distinguish between these alternatives are described in the accompanying paper (27).
Published Version
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