Effect of aminoglycoside otic drops on isolated cochlear outer hair cells with and without liver extract activation.

Objective: To assess the ototoxicity of commercially available Gentacidin and TobraDex ear drops with and without liver extract activation using isolated cochlear outer hair cells (OHCs).

Material And Methods: OHCs from adult chinchilla cochleae were exposed to standard bathing solution (SBS), liver extract alone and Gentacidin and TobraDex ear drops with and without liver extract. All experiments were performed at an osmolality of 305 +/-5 mOsm, at room temperature and for up to 60 min.

Effect of corticosteroid on salicylate-induced morphological changes of isolated cochlear outer hair cells.

Our previous studies showed that pretreatment with corticosteroids, which inhibits release of arachidonic acid (precursor of prostaglandins and leukotrienes), partially prevented salicylate-induced hearing loss in vivo. The purpose of this study was to determine the effect of pretreatment with corticosteroid (dexamethasone sodium phosphate) on isolated cochlear outer hair cells (OHCs) exposed to salicylate in vitro. Isolated OHCs from the chinchilla cochlea were exposed to salicylate with or without pretreatment with dexamethasone.

Protective effect of corticosteroid against the cytotoxicity of aminoglycoside otic drops on isolated cochlear outer hair cells.

Objectives: Otic drops are commonly used not only for otitis externa but also for otorrhea in the presence of tympanic membrane perforation or tympanostomy tube. Many studies demonstrated the ototoxicity of aminoglycoside. In our previous study, we observed that gentamicin (GM), when activated with liver extract, demonstrated significant cytotoxicity.

Effect of platelet activating factor with and without receptor antagonist (WEB2170) on morphology of isolated cochlear outer hair cells.

Platelet activating factor (PAF), generated from biologically active phospholipids, has been implicated as a potent inflammatory mediator and has been shown to be involved in many pathological processes, especially in inflammation and allergy. It has been suspected that PAF may be one of the inflammatory mediators in middle ear effusion that can induce sensorineural hearing loss, as observed in chronic otitis media. The PAF receptor antagonist WEB2170 has been studied extensively, and its inhibitory effects against various PAF actions are well proven in otologic systems.

Effect of nitric oxide on mucin production in experimental otitis media.

Objective: The purpose of this study was to determine the role of nitric oxide (NO) in the pathogenesis of mucoid otitis media (OM) in lipopolysaccharide (LPS)-induced OM.

Methods: OM was induced in chinchillas by injecting S-nitroso-N-acetylpenicillamine (SNAP), LPS, and LPS + SNAP into the superior bullae. Auditory brainstem response thresholds were measured every 24 hours.

Effects of nitric oxide on morphology of isolated cochlear outer hair cells: possible involvement in sensorineural hearing loss.

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.

Effect of round window membrane application of nitric oxide on hearing and nitric oxide concentration in perilymph.

Nitric oxide (NO), a free radical, has been found to be important in the development of middle ear effusions. However, the effect of NO in the middle ear effusion on cochlear function and on perilymph concentrations of NO has not been reported. We placed S-nitroso-N-acetylpenicillamine (SNAP), a NO donor compound, on the round window membrane (RWM) of adult chinchillas.