Pharmacological studies on the release of slow reacting substance of anaphylaxis during anti-immunoglobulin E antibody mediated passive peritoneal anaphylaxis in rats.

Abstract

The release of slow reacting substance of anaphylaxis (SRS-A) by anti-immunoglobulin E(IgE; epsilon)-antibody mediated passive peritoneal anaphylaxis (PPA) in rats was investigated immunopharmacologically. A significant amount of SRS-A was released by anti-epsilon-antibody in the peritoneal cavity of rats passively sensitized with IgE. The amount of SRS-A released by anti-epsilon-antibody was about one third less than that released in an anti-gamma-antibody and IgG2a system. The release of SRS-A was initiated at 2 min and reached its maximum 5 to 10 min after the injection of anti-epsilon-antibody. Disodium cromoglycate, tranilast and ketotifen inhibited the release of both SRS-A and histamine caused by anti-epsilon-antibody mediated PPA. Glucocorticoids (hydrocortisone, prednisolone and dexamethasone) also inhibited the release of both mediators. rho-Bromophenacyl bromide inhibited the release of both mediators. AA-861, a potent 5-lipoxygenase inhibitor, inhibited the release of SRS-A but not histamine. Indomethacin slightly enhanced the release of SRS-A and inhibited the release of histamine. Cytarabine resulted in leucopenia and inhibited the release of histamine but not SRS-A during PPA. Dextran sulfate reduced the number of glass adherent peritoneal cells and inhibited the release of SRS-A but not histamine. These results suggest the suitability of anti-epsilon-antibody mediated rat PPA for investigating the effect of anti-allergic agents on the release of SRS-A.