PROSTAGLANDIN E2, PROSTAGLANDIN I2 AND THE VASCULAR CHANGES OF INFLAMMATION

Abstract

Plasma exudation and blood flow changes induced by intradermal injection of prostaglandins E 2 (PGE 2), I 2 (PGI 2), D 2 (PGD 2) and F 2α (PGF 2α) were measured in rabbit dorsal skin by the use of [131 I]‐albumin and 133 Xe. Little plasma exudation was produced by any of the prostaglandins when injected alone. Both PGE 2 and PGI 2 were potent at increasing blood flow, whereas PGF 2α and PGD 2 produced an increase only at high doses. All of the prostaglandins studied potentiated the plasma exudation induced by bradykinin. PGE 2 and PGI 2 had similar potent potentiating activity, whereas PGD 2 and PGF 2ae had activity at doses too high to be of biological significance. Intradermal injections of arachidonate alone resulted in little plasma exudation but produced an increase in blood flow. Arachidonate potentiated bradykinin‐induced plasma exudation. Locally‐injected indomethacin had no effect on basal blood flow and little effect on the exudation produced by bradykinin, but indomethacin did inhibit the vasodilatation and exudation potentiation produced by arachidonate. PGE 2 and PGI 2 had similar potency in producing marked potentiation of plasma exudation induced by intradermal injection of zymosan. In the reaction to zymosan, it is concluded that vasodilatation is the result of the release of arachidonate, which is subsequently converted to either PGE 2 or PGI 2. These substances regulate the plasma exudation induced by independently‐released vascular permeability‐increasing mediators.