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- Publisher
- American Medical Association
- Copyright
- Copyright © 1997 American Medical Association. All Rights Reserved.
- ISSN
- 0886-4470
- eISSN
- 1538-361X
- DOI
- 10.1001/archotol.1997.01900010049006
- Publisher site
- See Article on Publisher Site
Abstract
Abstract 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 introduction 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 μLbetween 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.Arch Otolaryngol Head Neck Surg. 1997;123:41-46 References 1. Bluestone CD, Klein JO, Paradise JL, et al. Workshop on the effects of otitis media on the child . Pediatrics . 1983;71:639-652. 2. 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A mechanism for the antiinflammatory effects of corticosteroids: the glucocorticoid receptor regulates leukocyte adhesion to endothelial cells and expression of endothelialleukocyte adhesion molecule 1 and intercellular adhesion molecule 1 . Proc Natl Acad Sci U S A . 1992;89:9991-9995.Crossref 18. Kolls J, Xie J, LeBlanc R, et al. Rapid induction of messenger RNA for nitric oxide synthase II in rat neutrophils in vivo by endotoxin and its suppression by prednisolone . Proc Soc Exp Biol Med . 1994;205:220-225.Crossref 19. Balligand J, Ungureanu-Longrois D, Simmons WW, et al. Cytokine-inducible nitric oxide synthase (iNOS) expression in cardiac myocytes . J Biol Chem . 1994; 269:27580-27588. 20. Vidal MJ, Zocchi MR, Poggi A, Pellegatta F, Chierchia SL. Involvement of nitric oxide in tumor cell adhesion to cytokine-activated endothelial cells . J Cardiovasc Pharmacol . 1992;20( (suppl 12) ):S155-S159.Crossref 21. Boschetto P, Rogers DF, Fabbri LM, Barnes PJ. 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Journal
Archives of Otolaryngology - Head & Neck Surgery – American Medical Association
Published: Jan 1, 1997
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