Prostaglandins as Potentiators of Increased Vascular Permeability in Inflammation

Abstract

PROSTAGLANDINS are released in inflammatory reactions in animals¹ and in man². The observation that non-steroidal anti-inflammatory agents inhibit prostaglandin synthesis in vitro^3,4 and in vivo⁵, and that the comparative potency of these anti-inflammatory compounds is the same in vitro and in vivo as inhibitors of carrageenin-induced oedema⁶, suggests that prostaglandins may have an important role in inflammation. Prostaglandins (E₁, E₂, F_1α and F_2α) evoke increased vascular permeability in the skin of rat and man⁷, which appears to be an indirect effect resulting from mast cell degranulation. The lack of potency of prostaglandins in causing increased vascular permeability on intradermal injection in the guinea pig⁸ has, however, received little attention. We have confirmed this observation (Fig. 1, Table 1) and conclude that in the guinea pig prostaglandins cannot be regarded as chemical mediators which act directly on the vascular endothelium as do histamine, serotonin (5-hydroxytryptamine) and bradykinin. We have therefore investigated a possible alternative role for prostaglandins in inflammatory mechanisms.