Acta oto-laryngologica
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Acta oto-laryngologica · Mar 1997
On the function of the pars flaccida: retraction of the pars flaccida and buffering of negative middle ear pressure.
Retraction of the elastic pars flaccida (PF) is the first reaction to a middle ear (ME) negative pressure in adults. Such retraction reduces middle ear volume, thereby elevating the ambiant pressure. PF retraction acts therefore as a buffering mechanism which counteracts ME negative pressure. ⋯ It was calculated that retraction of the PF stage I and II may counteract 1-80 mm H2O of negative ME pressure-depending on the degree of retraction and the extent of mastoid pneumatization. The range of PF retraction suggests that normal pressure in the ME fluctuates, up to 8 mm H2O in average pneumatic ears (10 cm2) extending eventually to 80 mm2 in ears with sclerotic mastoids. Other mechanisms which may also serve the ME as pressure buffers by reducing its volume-once a negative pressure sets in-are retraction of the pars tensa, swelling of the mucosa or flooding the ME cavity with an exudate.
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Acta oto-laryngologica · Sep 1996
Recording from the inferior colliculus following cochlear inner hair cell damage.
The anti-cancer drug carboplatin has been used to generate inner hair cell (IHC) lesions in the cochleae of chinchilla. This model has provided a valuable physiological tool for the study of the auditory system, particularly concerning the relative roles of IHCs and outer hair cells (OHCs). ⋯ No evoked afferent responses could be detected in CN regions which represented cochlear loci where total IHC loss had occurred. Normal frequency selectivity in the auditory system is possible with small numbers of surviving IHCs provided OHCs remain normal.
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Acta oto-laryngologica · Jul 1996
Sodium and potassium currents of type I spiral ganglion cells from rat.
Ion channel activity of acutely dissociated type I spiral ganglion cells isolated from rats was investigated using the whole-cell variation of the patch clamp technique. Tetrodotoxin-sensitive sodium current and tetraethylammonium-sensitive potassium current were recorded. With a holding potential of -80 mV, peak sodium currents were generated by depolarizations to membrane potentials more positive than -50 mV. ⋯ Steady-state sodium channel inactivation curve yielded a slope of 12 mV and a half-inactivated potential of -83 mV. Recovery from inactivation of the sodium channel proceeded with a fast and slow time course; recovery began as early as 0.8 ms and proceeded with a time constant of 7.5 ms. It is concluded that type I spiral ganglion cells are endowed with sodium and potassium channels which are responsible for generation and propagation of auditory nerve action potentials.
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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.