vasoactive-intestinal-peptide and Ear-Diseases

The general pattern of local inflammation in the rat is developed in the pad of the paw. In otorhinolaryngology a model of local inflammation can be reached in the rat ear by means of the production of an auricular chondritis. For that, we have protocolized the methodology. The induction of inflammation is carried out by the substance vegetable carrageenan. It has been verified by histological studies the inflammation generated, as well as studying the action of antiinflammatory, proinflammatory and inflammatory compounds. The inflammation has been measured by nonius and by determination of the activity of the myeloperoxidase enzyme. After these studies we can validate the auricular chondritis in rat as an experimental model of local inflammation in otorhinolaryngology.

Topics: Animals; Cartilage; Disease Models, Animal; Ear Diseases; Ear, External; Female; Inflammation; Rats; Rats, Wistar; Vasoactive Intestinal Peptide

We have investigated the effects of actinomycin D on mouse ear oedema induced by capsaicin, neuropeptides, and established inflammatory mediators. Actinomycin D (0.5 mg/kg, i.v.) significantly (P < 0.01) inhibited ear oedema induced by topical application of capsaicin, while adriamycin (6.0 mg/kg, i.v.) and cycloheximide (6.0 mg/kg, i.v.) had no effect on oedema. The ear oedema induced by intradermal injection of neuropeptides such as mammalian tachykinins, calcitonin gene-related peptide (CGRP), and vasoactive intestinal peptide (VIP), was markedly (P < 0.05, P < 0.01 or P < 0.001) suppressed by actinomycin D. The drug was also effective (P < 0.01 or P < 0.001) in inhibiting bradykinin (BK)- and compound 48/80-induced ear oedema, but did not inhibit oedema induced by histamine, 5-HT, leukotriene C4 (LTC4), and platelet activating factor (PAF) at a dose of 1 mg/kg. In mast cell-deficient W/WV mice, actinomycin D (1.0 mg/kg, i.v.) failed to inhibit substance P (SP)-induced ear oedema whereas spantide (0.5 mg/kg, i.v.) was an effective (P < 0.01) inhibitor of oedema formation. Furthermore, actinomycin D (10-100 microM) dose-dependently prevented histamine release from rat peritoneal mast cells evoked by SP, compound 48/80, and the ionophore A23182, respectively. These results strongly suggest that an inhibitory effect of actinomycin D on neurogenic inflammation is due primarily to the prevention of mast cell activation mediated by neuropeptides, rather than an interaction with DNA or receptors of neuropeptides.

Topics: Animals; Bradykinin; Calcimycin; Calcitonin Gene-Related Peptide; Capsaicin; Cycloheximide; Dactinomycin; Disease Models, Animal; Dose-Response Relationship, Drug; Doxorubicin; Ear Diseases; Edema; Histamine; Injections, Intravenous; Leukotriene C4; Male; Mast Cells; Mice; p-Methoxy-N-methylphenethylamine; Platelet Activating Factor; Rats; Rats, Wistar; Serotonin; Substance P; Tachykinins; Vasoactive Intestinal Peptide