We have previously characterized the kinetics of prostaglandin D2 (PGD2) production at cutaneous sites of allergic inflammation employing a blister-chamber model. In this study, a more complete profile of prostaglandins released in vivo was obtained. PGD2 release, as measured by radioimmunoassay and by combined gas chromatography-mass spectrometry, was evident within 1 h after antigen challenge with maximal levels occurring 3-4 h post-challenge. The 11-ketoreductase metabolite of PGD2, 9 alpha, 11 beta-prostaglandin F2 was present in blister fluid from three of six patients at the time of maximal levels of PGD2. The stable non-enzymatic hydrolysis product of prostacyclin, 6-keto-prostaglandin F1 alpha, was significantly elevated in blister fluid from five of six patients following antigen challenge. In these subjects, the levels of 6 kappa-PGF1 alpha were highest in samples obtained 1 and 2 h after antigen challenge and remained significantly elevated until 5 h post-challenge. Levels of prostaglandin E2, prostaglandin F2 alpha and thromboxane B2 did not vary significantly. These studies suggest that following antigen challenge two fatty-acid cyclo-oxygenase products of arachidonic acid are released, PGD2 and prostacyclin. The 11-ketoreductase metabolism of PGD2 to 9 alpha, 11 beta-PGF2 could represent a mechanism by which the biological effects of PGD2 are prolonged in cutaneous tissue. The presence of 6 kappa-PGF1 alpha in the blister fluid suggests that significant prostacyclin release occurs as the result of antigen challenge and could represent a mechanism by which the prolonged microvascular response in cutaneous tissue may occur.