Anaphylaxis increases 8-iso-prostaglandin F2α release from guinea-pig lung in vitro

8-Iso-prostaglandin F-2 alpha release from isolated and perfused guinea-pig lung was measured by radioimmunoassay. 8-Iso-prostaglandin F-2 alpha release was detectable under basal conditions and increased 10-fold during antigen-induced bronchoconstriction, concomitant with the increase of thromboxane B-2 and prostaglandin E-2. The anti-8-iso-prostaglandin F-2 alpha serum used in the radioimmunoassay seems to be quite specific for this compound. Pretreatment of lungs with indomethacin (a non-selective inhibitor of cyclooxygenase) reduced 8-iso-prostaglandin F-2 alpha release under basal conditions and completely abolished the increase observed during lung anaphylaxis. Pretreatment of lungs with NS 398 (N-[2-cyclohexyl]-4-nitrophenyl methanesulphonamide), a selective inhibitor of cyclooxygenase-2, did not change basal or antigen-induced 8-iso-prostaglandin F-2 alpha release at all. We conclude that under basal conditions guinea-pig lung perfusates contain low levels of 8-iso-prostaglandin F-2 alpha-like immunoreactivity, which increase 10-fold during antigen-induced bronchoconstriction. This isoprostane seems to be derived from the cyclooxygenation of arachidonic acid via the constitutive form of cyclooxygenase. (C) 1999 Elsevier Science B.V. All rights reserved.