OBJECTIVE: To determine the role of nitric oxide (NO) and peroxynitrite on mucociliary activity in experimental otitis media with effusion (OME). STUDY DESIGN AND SETTING: Twenty guinea pigs were divided into 1 control and 3 experimental groups; lipopolysaccharide (LPS), N(G)-nitro-L-arginine methyl ester (L-NAME), and uric acid (UA) groups. Ten ears were used in each group. OME was induced by transtympanic injection of LPS in experimental groups. Twenty-four hours after the transtympanic injection, dye transfer time (DTT) was measured and the temporal bone was taken for histopathologic examination. Expression of peroxynitrite was determined by immunohistochemical stain for 3-nitrotyrosine (3-NT). RESULTS: Dye transfer time was significantly delayed in LPS group compared to control group; by contrast it was significantly reduced in L-NAME or UA treated groups (P < 0.01). Histopathologic examination showed reduced inflammation and mucosal thickening in the treatment groups when compared to LPS group. These findings, however, were not statistically significant. Immunoreactivity to 3-NT was intense in LPS group and decreased in the treatment groups (P < 0.05). CONCLUSIONS: It is suggested that LPS induced mucociliary dysfunction in the middle ear by NO and peroxynitrite-mediated pathways.
OBJECTIVE: To determine the role of nitric oxide (NO) and peroxynitrite on mucociliary activity in experimental otitis media with effusion (OME). STUDY DESIGN AND SETTING: Twenty guinea pigs were divided into 1 control and 3 experimental groups; lipopolysaccharide (LPS), N(G)-nitro-L-arginine methyl ester (L-NAME), and uric acid (UA) groups. Ten ears were used in each group. OME was induced by transtympanic injection of LPS in experimental groups. Twenty-four hours after the transtympanic injection, dye transfer time (DTT) was measured and the temporal bone was taken for histopathologic examination. Expression of peroxynitrite was determined by immunohistochemical stain for 3-nitrotyrosine (3-NT). RESULTS: Dye transfer time was significantly delayed in LPS group compared to control group; by contrast it was significantly reduced in L-NAME or UA treated groups (P < 0.01). Histopathologic examination showed reduced inflammation and mucosal thickening in the treatment groups when compared to LPS group. These findings, however, were not statistically significant. Immunoreactivity to 3-NT was intense in LPS group and decreased in the treatment groups (P < 0.05). CONCLUSIONS: It is suggested that LPS induced mucociliary dysfunction in the middle ear by NO and peroxynitrite-mediated pathways.
Authors: Steven K Juhn; Min-Kyo Jung; Mark D Hoffman; Brian R Drew; Diego A Preciado; Nicholas J Sausen; Timothy T K Jung; Bo Hyung Kim; Sang-Yoo Park; Jizhen Lin; Frank G Ondrey; David R Mains; Tina Huang Journal: Clin Exp Otorhinolaryngol Date: 2008-09-30 Impact factor: 3.372