Suppression by prostaglandin E1 of vascular permeability induced by vasoactive inflammatory mediators.

Abstract

Abstract Systemic treatment of rats with prostaglandin E1 or with its stable derivative, 15-(S)-15-methyl-Prostaglandin E1, markedly reduce the increases in vasopermeability induced by the intradermal injection of histamine, serotonin, bradykinin, C3a, and compound 48/80. This inhibition is dependent on the dose of the vasopermeability factor and the duration of time between injection of the prostaglandin and intradermal injection of vasopermeability factor. The inhibition of associated ultrastructurally with a preservation of tight junctions between endothelial cells. The structure-function specificity of the inhibitory effects of the prostaglandin is shown by the diminished effects of prostaglandin A2, and the lack of inhibition by prostaglandin F2 alpha. These data provide evidence that PGE1 interferes with the local effects of vasopermeability mediators and may explain the earlier observations at PGE1 protects animals from immune complex-induced nephritis.