Objective: To understand the actions of glucocorticoids on the development and progression of endotoxin mediated otitis media with effusion. Methods and Design: The middle ears of 20 Sprague-Dawley rats were exposed to 35 μL of either 300-mOsm Krebs-Ringer solution (control: n=5) or lipopolysaccharide, 1 mg/mL, dissolved in Krebs-Ringer solution (n=15). Among the group that received lipopolysaccharide, 10 rats were randomly selected to receive dexamethasone (1 mg/kg intramuscularly), either 2 hours (n=5) or 24 hours (n=5) before the production of lipopolysaccharide. Middle ear fluid was sampled after 2, 4, and 6 hours of exposure. Outcome Measures: Middle ear fluid volume and albumin content were determined as measures of vascular extravasation. Histological sections of the middle ear mucosa were used to quantify the degree of leukocyte exudation. Data were analyzed by 1- or 2- way analysis of variance with the significance level set at P<.05. Results: Lipopolysaccharide exposure caused a significant increase in the mean±SEM middle ear fluid volume from 29.9±0.99 to 45.8±1.4 μL between the 2- and 6-hour samplings. Lipopolysaccharide exposure caused a significant increase in the albumin content of middle ear fluid from 70.1±19.2 to 271.0±93.1 μg between the 2- and 6-hour samplings. Both increases were significant compared with controls. Lipopolysaccharide also caused a significant increase in leukocytes localized to the middle ear mucosa. Pretreatment of animals with dexamethasone for either 2 or 24 hours inhibited the lipopolysaccharide- induced changes. There were no differences between 2- and 24-hour pretreatment with dexamethasone. Conclusions: Dexamethasone inhibits the development of endotoxin-induced otitis media with effusion.
|Original language||English (US)|
|Number of pages||6|
|Journal||Archives of Otolaryngology--Head and Neck Surgery|
|State||Published - Jan 1997|
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