ARACHIDONIC-ACID METABOLITES IN EXPERIMENTAL OTITIS-MEDIA AND EFFECTSOF ANTIINFLAMMATORY DRUGS

Previous studies have shown that arachidonic acid (AA) metabolites are important in the pathogenesis of otitis media with effusion. The AA m etabolites in 4 different experimental models for otitis media were an alyzed, and the effect of anti-inflammatory drugs was studied. Purulen t odds media was induced in rats by inoculation of Streptococcus pneum oniae in the tympanic bulla, serous otitis media by blocking the tympa nal orifice of the eustachian tube, and mucoid odds media by combining the two procedures. Middle ear effusion was also induced by stimulati ng the external auditory canal with cold air. Indomethacin and hydroco rtisone were used to inhibit AA metabolism in the latter model. Lipoxy genase products dominated in the purulent and cold air otitis media mo dels. Cyclooxygenase products dominated in the mucoid and serous model s. Indomethacin inhibited accumulation of middle ear effusion in the c old air odds media model whereas hydrocortisone did not. Apart from AA metabolites, other mechanisms and mediators appear to be responsible for the increased vessel permeability observed in the cold air otitis media model, such as interactions between mast cells and nerves in the middle ear mucosa.