Treatment of Acoustic Trauma

D'Aldin, Christine; Cherny, Lily; Devriere, F.; Dancer, A.

doi:10.1111/j.1749-6632.1999.tb08652.x

Cited by 36 publications

(65 citation statements)

References 18 publications

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“…It is assumed that the C02, in carbogen acts synergistically with oxygen in carbogen to produce increased oxygenation of cochlear tissues and to reduce cochlear damage. However, as previously reported by Hatch et al [44], d'Aldin et al [36] observed no significant difference between the carbogen-treated animals after the noise exposure and the control group. Therefore, carbogen could have a protective effect, but with much less curative efficiency.…”

Section: Discussionsupporting

confidence: 55%

“…However, Lamm and Arnold [41] observed that an improvement in cochlear blood flow is not necessarily associated with improvement of auditory function.. At 2 ATA hyperbaric oxygen, the amount of oxygen and blood-dissolved oxygen fraction available are multiplied by 10. In the study of d'Aldin et al [36], no improvement in threshold shifts can be observed, however, under those hyperbaric conditions. On the contrary, either at 2.5 or 1.5 ATA, hyperbaric oxygen treatment results in a higher threshold shift and additional hair cell damage.…”

Section: Hyperbaric Oxygen Therapymentioning

confidence: 81%

“…The actual efficiency of the classical medical treatments of the acoustic trauma was assessed by using a wellstandardized animal study by d'Aldin et al [36]. The results are related to the effect of the most widely used medical treatments.…”

Section: Methodsmentioning

confidence: 99%

“…Improvement in threshold shifts is reported only when pure oxygen is given during noise exposure [44]. Accordingly, the effectiveness of oxygen delivered at the ambient pressure level after intense noise exposure is not shown in the study of d'Aldin et al [36].…”

Section: Isobaric Oxygen Therapymentioning

confidence: 95%

“…At this point we have to remind that dAldin et al [34] and Puel et al [35] demonstrated that dendritic damage at the base of inner hair cells, the latter representing the site of CAP generation, accounts for half the contribution to acute hearing loss after acoustic trauma (especially in case of continuous noise exposure). In the long term study of d'Aldin et al [36], when the first injection of corticoid is given 1 h or 24 hours after exposure to noise, noise-induced threshold shift is decreased, recovery is faster, and less hair cell damage is observed (noise-induced hearing loss observed one day after corticoid administration: 25 dB, is almost equivalent to that observed 14 days after exposure in untreated animals: 20 dB). Thus, it seems that corticoid acts both at the dendritic and the cellular level.…”

Section: Hyperbaric Oxygen Therapymentioning

confidence: 96%

See 4 more Smart Citations

Damage Risk from Impulse Noise. (les Risques auditifs et extra auditifs des bruits impulsionnels)

H¹,

Johnson²,

Buck³

et al. 2000

PsycEXTRA Dataset

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Section: Discussionsupporting

confidence: 55%

Section: Hyperbaric Oxygen Therapymentioning

confidence: 81%

Section: Methodsmentioning

confidence: 99%

Section: Isobaric Oxygen Therapymentioning

confidence: 95%

Section: Hyperbaric Oxygen Therapymentioning

confidence: 96%

See 3 more Smart Citations

Damage Risk from Impulse Noise. (les Risques auditifs et extra auditifs des bruits impulsionnels)

H¹,

Johnson²,

Buck³

et al. 2000

PsycEXTRA Dataset

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NF‐κB mediated glucocorticoid response in the inner ear after acoustic trauma

Tahera

Meltser

Johansson

et al. 2006

J of Neuroscience Research

111

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The inner ear of humans and experimental animals demonstrate an abundance of glucocorticoid receptors (GR). Glucocorticoids (GC) are widely used to treat different hearing disorders; yet the mechanisms of GC action on the inner ear are unknown. We demonstrate how GR can directly modulate hearing sensitivity in response to a moderate acoustic trauma that results in a hearing loss (10-30 dB). The GC agonist (dexamethasone) and the drugs (metyrapone + RU 486) showed opposing effects on hearing threshold shifts. GC agonist (dexamethasone) decreased the hearing threshold whereas pre-treatment with a GC synthesis inhibitor (metyrapone) in combination with a GR antagonist (RU 486) exacerbated auditory threshold shifts (25-60 dB) after acoustic trauma with statistically significant increase in GR mRNA and GR protein compared with the vehicle and acoustic trauma group. Acoustic trauma caused a significant increase in the nuclear transport of NF-kappaB, whereas pre-treatment with the drugs (metyrapone and RU 486) blocked NF-kappaB nuclear transport into spiral ganglion nuclei. An NF-kappaB inhibitor, pyrrolidine dithiocarbamate ammonium blocked the trauma-induced translocation of NF-kappaB and resulted in a hearing loss (45-60) dB. These results indicate that several factors define the responsiveness of the inner ear to GC, including the availability of ligand or receptor, and the nuclear translocation of GR and NF-kappaB. These findings will further our understanding of individual GC responsiveness to steroid treatment, and will help improve the development of pharmaceuticals to selectively target GR in the inner ear for individuals with increased sensitivity to acoustic trauma.

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Macrophage contribution to the response of the rat organ of Corti to amikacin

Ladrech

Wang

Simonneau

et al. 2007

J of Neuroscience Research

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Transdifferentiation of nonsensory supporting cells into sensory hair cells occurs naturally in the damaged avian inner ear. Such transdifferentiation was achieved experimentally in the cochlea of deaf guinea pigs through Atoh 1 gene transfection. Supporting cells may therefore serve as targets for transdifferentiation therapy. Supporting cells rapidly degenerate after hair cell disappearance, however, limiting the therapeutic window for gene transfer. We studied the time course of ultrastructural and phenotypical changes occurring in Deiters cells (hair cell supporting cells) after ototoxic treatment in the rat. The presence of macrophages in the cochlea was also investigated, to study any deleterious effects they may have on pathologic tissues. One week after treatment most hair cells had disappeared. Deiters cells no longer expressed the glial marker vimentin but instead displayed typical hair cell markers, the calcium binding proteins calbindin and parvalbumin. This suggests that a process of transdifferentiation of Deiters cells into hair cells was activated. By 3 weeks post-treatment, however, the Deiters cells began to degenerate and by 10 weeks post-treatment the organ of Corti was degraded fully. Interestingly, a marked increase in macrophage density was seen after the end of amikacin treatment to 10 weeks post-treatment. This suggests chronic inflammation is involved in epithelium degeneration. Consequently, early treatments with anti-inflammatory factors might promote supporting cell survival, thus improving the efficacy of more specific strategies aimed to regenerate hair cells from nonsensory cells.

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Treatment of Acoustic Trauma

Cited by 36 publications

References 18 publications

Damage Risk from Impulse Noise. (les Risques auditifs et extra auditifs des bruits impulsionnels)

Damage Risk from Impulse Noise. (les Risques auditifs et extra auditifs des bruits impulsionnels)

NF‐κB mediated glucocorticoid response in the inner ear after acoustic trauma

Macrophage contribution to the response of the rat organ of Corti to amikacin

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