Inhibition by non-steroid anti-inflammatory agents of rabbit aorta contracting activity generated in blood by slow reacting substance C.

1 A crude and a partially purified preparation of slow reacting substance C (SRS-C) as well as arachidonic acid decreased resistance to perfusion of the dog hind paw. This effect was suppressed by treatment with non-steroid anti-inflammatory drugs.2 Injections of SRS-C or of arachidonic acid induced marked and reproducible contractions of strips of rabbit aorta and a rat stomach which were bathed in blood from an anaesthetized dog. The effect on the rabbit aorta is attributed to formation of a rabbit aorta contracting substance (RCS). The contractions were suppressed when the dog was treated with a non-steroid anti-inflammatory drug.3 Incubation of blood or of platelet-rich plasma with SRS-C or arachidonic acid resulted in the formation of similar materials. This formation was suppressed by anti-inflammatory drugs.4 SRS-C, linoleic, linolenic, and arachidonic acids are suitable substrates for soybean lipoxidase for the generation of RCS.5 It is suggested that RCS and prostaglandin are formed within platelets, when SRS-C or arachidonic acid are injected into animals or added in vitro. Non-steroid anti-inflammatory drugs suppress these effects, possibly by inhibiting prostaglandin synthetase.