Noise-induced Vasoconstriction in the Cochlea

Nakai, Yousuke; Masutani, Haruhiko

doi:10.3109/00016488809102853

Cited by 30 publications

(17 citation statements)

References 6 publications

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“…Although fixation may induce variation in strial capillary lumenal diameter, this was not observed in control tissues. Increased capillary lumenal diameters following noise exposure and fixation have been reported previously [41] and by casting techniques [42]. Intriguingly, vasodilation is not a prerequisite of sound-enhanced trans-strial trafficking.…”

Section: Discussionmentioning

confidence: 76%

Acoustic Trauma Increases Cochlear and Hair Cell Uptake of Gentamicin

Wang

Steyger

2011

PLoS ONE

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BackgroundExposure to intense sound or high doses of aminoglycoside antibiotics can increase hearing thresholds, induce cochlear dysfunction, disrupt hair cell morphology and promote hair cell death, leading to permanent hearing loss. When the two insults are combined, synergistic ototoxicity occurs, exacerbating cochlear vulnerability to sound exposure. The underlying mechanism of this synergism remains unknown. In this study, we tested the hypothesis that sound exposure enhances the intra-cochlear trafficking of aminoglycosides, such as gentamicin, leading to increased hair cell uptake of aminoglycosides and subsequent ototoxicity.MethodsJuvenile C57Bl/6 mice were exposed to moderate or intense sound levels, while fluorescently-conjugated or native gentamicin was administered concurrently or following sound exposure. Drug uptake was then examined in cochlear tissues by confocal microscopy.ResultsProlonged sound exposure that induced temporary threshold shifts increased gentamicin uptake by cochlear hair cells, and increased gentamicin permeation across the strial blood-labyrinth barrier. Enhanced intra-cochlear trafficking and hair cell uptake of gentamicin also occurred when prolonged sound, and subsequent aminoglycoside exposure were temporally separated, confirming previous observations. Acute, concurrent sound exposure did not increase cochlear uptake of aminoglycosides.ConclusionsProlonged, moderate sound exposures enhanced intra-cochlear aminoglycoside trafficking into the stria vascularis and hair cells. Changes in strial and/or hair cell physiology and integrity due to acoustic overstimulation could increase hair cell uptake of gentamicin, and may represent one mechanism of synergistic ototoxicity.

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Section: Discussionmentioning

confidence: 76%

Acoustic Trauma Increases Cochlear and Hair Cell Uptake of Gentamicin

Wang

Steyger

2011

PLoS ONE

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“…These results point to a noise-induced cochlear metabolic disturbance or to a me chanical lesion producing hearing loss. A declined blood flow in the basal turn of the guinea pig's cochlea after 1 h exposure to a 12-kHz tone has been demonstrated using a laser Doppler flowmeter [20], as well as a noise-induced vasoconstriction in the cochlea using a blood vessel casting method and scanning electron microscopy [21 ].…”

Section: Discussionmentioning

confidence: 99%

Morphologic Damage and Changes of Intracellular Calcium-Binding Sites after Acute Noise Trauma in the Organ of Corti of the Guinea Pig

Maurer¹,

Heinrich²,

Mann³

1993

ORL

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In guinea pigs, an acute acoustic trauma was created by 6 consecutive gunshots. The sound pressure at the ear drum was 156 ± 4 dB, the frequency maximum was between 4 and 6 kHz. Sixty hours after the noise trauma, the animals were decapitated, and the cochleae were prepared for microscopic analysis of the resulting trauma to the organ of Corti. During the process of fixation, the potassium-pyroantimonate precipitation reaction was performed to localize calcium-binding sites. The pattern of cell morphology and the distribution of calcium-binding sites was compared to that of normal control animals. Morphologic changes of the cells in the organ of Corti correlated with changes of the cellular calcium distribution, indicating the crucial role of calcium in cell damage and necrosis after acute noise trauma.

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“…Much of this hearing loss is thought to occur in the peripheral organ. The mechanisms may include synaptic fatigue (Mulroy et al, 1990), metabolic fatigue of either the stria vascularis or hair cells (Canlon and Schacht, 1983), changes in cochlear blood flow (Nakai and Masutani, 1988) and non-detectable morphological disruption of mechanoelectrical channels (Patuzzi, 1998).…”

Section: Introductionmentioning

confidence: 99%