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Background and Objectives:Nitric oxide (NO)NO is an important mediator in the pathogenesis of otitis media with efusion. The harmful efect of NO is related with NO-derived intermediates such as peroxynitrite (OONO-). The author investigated the role of NO and peroxynitrite on mucociliary activity in experimental otitis media with efusion. Materials and Method:Otitis media with efusion was induced by injecting lipopolysacharide (LPS) transtympanically in guinea pigs. In the NG-nitro-L-arginine methyl ester (L-NAME) group, L-NAME was additionally injected intratympanicaly and intramuscularly. Uric acid (UA) group was treated with intraperi-toneal injection of UA 3 times. After 24 hours, dye transfer time was measured and temporal bones were taken for histopathologic examination. Expresion of peroxynitrite was determined by imunohistochemical stain for 3-nitrotyrosine (3-NT). Results:Transfer time of dye was prolonged in LPS group, whereas it was significantly reduced in L-NAME or UA not statisticaly significant. 3-NT was expresed intensely in subepithelial layer of LPS group, and decreased to mild to moderate degree in the treatment groups. Conclusion:LPS induced mucociliary dysfunction in the middle ear by NO and peroxynitrite-mediated pathways. This study sugests that inhibition of NO synthesis or scavenging of peroxynitrite may have an adjunctive role in the future treatment of otitis media with efusion. (Korean J Otolaryngol 203 ;46 :720-6)