Acta oto-laryngologica
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Acta oto-laryngologica · May 1996
Comparative StudyOtoacoustic emission amplification after inner hair cell damage.
Otoacoustic emissions (OAEs) are considered to originate from active cochlear processes involving the outer hair cells (OHC). These emissions are suppressed by activity in the efferent olivocochlear bundle (OCB) and following OHC damage caused by noise exposure or ototoxic drugs. Temporary enhancement of OAEs may occur following noise exposure, and permanent enhancement of emissions has been associated with primary afferent dysfunction in the auditory system. ⋯ These results support the theory that OHCs cells are involved in the production of these cochlear emissions but also provides further evidence that active adaptation processes exist in the cochlea. It is postulated that loss of afferent input reduces the activity in the medial efferent OCB resulting in de-suppression of OHC contractility. Enhanced OHC contractility could then produce amplification of CEOAEs.
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Acta oto-laryngologica · May 1996
Paranasal sinusitis after long-term use of topical nasal decongestants.
The aim of this study was to evaluate the incidence of paranasal sinusitis and the histologic changes in the sinus mucosa after long-term administration of topical nasal decongestants, phenylephrine and oxymetazoline. Experimental animals were divided into 3 groups for topical administration for 1 week, 2 weeks, and 4 weeks. Purulent maxillary sinusitis developed in 4 of 10 two-week phenylephrine group, 6 of 10 four-week phenylephrine group, 1 of 10 two-week oxymetazoline group and 3 of 10 four-week oxymetazoline group. ⋯ Ciliary loss was more prominent in the 4-week phenylephrine group than in the oxymetazoline group. Dilatation of mitochondria and vacuolization in cytoplasm were prominent in the 4-week groups with both phenylephrine and oxymetazoline. The results of this study suggest that the administration of decongestants may cause ciliary loss with subsequent sinusitis.