Pg. Goldie et al., ARACHIDONIC-ACID METABOLITES IN EXPERIMENTAL OTITIS-MEDIA AND EFFECTSOF ANTIINFLAMMATORY DRUGS, The Annals of otology, rhinology & laryngology, 102(12), 1993, pp. 954-960
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.