Hypothesis: One of the inflammatory mediators of otitis media, nitric oxide, can damage cochlear outer hair cells.
Background: Free radicals, including nitric oxide, have been detected in middle ear effusion. Increasing evidence implicates free radicals in the pathogenesis of otitis media and possibly in the development of sensorineural hearing loss.
Methods: Isolated outer hair cells from adult chinchilla cochlea were exposed to standard bathing solution (Control Group 1) or the nitric oxide-producing compounds, S-nitroso-N-acetyl, l-penicillamine (1-1.5 mg/ml, Experimental Group 1) or 3-morpholinosynonimine (1-1.5 mg/ml, Experimental Group 2). Since nitric oxide is readily converted to nitrite and nitrate in vivo, a second control group using sodium nitrite was used to separate potential effects of nitric oxide from nitrite (Control Group 2). All experiments were performed at an osmolality of 305 +/- 5 mOsm at room temperature, and with exposure time up to 90 minutes. The cells were observed using an inverted microscope, and the images were recorded and analyzed on the IMAGE Pro-Plus program.
Results: Outer hair cells exposed to either standard bathing solution or sodium nitrite (Control Groups 1 and 2) showed no significant change in cell shape or length. Cells exposed to S-nitroso-N-acetyl and l-penicillamine or 3-morpholinosynonimine exhibited ballooning and significant shortening in mean cell length (p < 0.01).
Conclusion: This study demonstrates that exposure to nitric oxide causes irreversible morphologic changes in isolated outer hair cells, suggesting possible involvement of nitric oxide radical in the development of sensorineural hearing loss as a sequela of chronic otitis media.