title: Inhibition of vascular permeability increase in mice. An additional anti-allergic mechanism of glucocorticoids.
abstract: Effects of glucocorticoids on IgE antibody-mediated 48-hour homologous passive cutaneous anaphylaxis (PCA) and skin reactions caused by mediator releasers and vascular permeability increasing factors were investigated comparatively. Both PCA and skin reactions were evoked in the mouse ear and these reactions were quantitatively evaluated by measuring the amount of dye extravasated into the ear. The glucocorticoids hydrocortisone, prednisolone and dexamethasone inhibited the PCA significantly. The maximum inhibitory effects of these glucocorticoids were obtained when administered 8 h prior to the antigenic challenge. Dexamethasone significantly inhibited the skin reactions caused by compound 48/80, Ca ionophore A 23187 and hypotonic salt solution. Dexamethasone also significantly inhibited the skin reactions caused by histamine, serotonin, platelet-activating factor, leukotrienes C4 and D4, and bradykinin. The maximum inhibitory effects of dexamethasone on these skin reactions were observed when administered 12-6 h before. These results support the previous observations that glucocorticoids inhibit the increase of vascular permeability caused by various stimuli, and indicate that the inhibition of vascular permeability increase contributes at least in part to the inhibitory effects on the PCA and the mediator releaser-induced skin reactions. Furthermore, the inhibition of vascular permeability increase by glucocorticoids might play an important role in their anti-allergic actions.
authors.affiliation: Department of Pharmacology, Gifu Pharmaceutical University, Japan.
authors.forename: N
authors.initials: N
authors.lastname: Inagaki
authors.forename: T
authors.initials: T
authors.lastname: Miura
authors.forename: H
authors.initials: H
authors.lastname: Nagai
authors.forename: Y
authors.initials: Y
authors.lastname: Ono
authors.forename: A
authors.initials: A
authors.lastname: Koda
mesh_terms: D000818:Animals; D002199:Capillary Permeability / Q000187:drug effects*; D003907:Dexamethasone / Q000494:pharmacology; D005260:Female; D005938:Glucocorticoids / Q000494:pharmacology*; D006854:Hydrocortisone / Q000494:pharmacology; D006967:Hypersensitivity / Q000188:drug therapy / Q000503:physiopathology*; D008222:Lymphokines / Q000494:pharmacology; D008297:Male; D051379:Mice; D008807:Mice, Inbred BALB C; D010323:Passive Cutaneous Anaphylaxis / Q000187:drug effects; D011239:Prednisolone / Q000494:pharmacology; D012867:Skin / Q000098:blood supply* / Q000187:drug effects / Q000276:immunology; D042461:Vascular Endothelial Growth Factor A; D042442:Vascular Endothelial Growth Factors
chemical_list: D005938:Glucocorticoids; D008222:Lymphokines; D042461:Vascular Endothelial Growth Factor A; D042442:Vascular Endothelial Growth Factors; D003907:Dexamethasone; D011239:Prednisolone; D006854:Hydrocortisone