Hair Cell Damage In The Guinea Pig Due To Different Kinds Of Noise

Erlandsson, B.; Håkanson, Håkan; Ivarsson, A; Nilsson, P; Wersäll, Jan

doi:10.3109/00016488009124953

Cited by 27 publications

(10 citation statements)

References 40 publications

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“…In 450 animals we have never found any signs of otitis media or hereditary disease and there is a very low spontaneous hair cell loss. Details of the exposures and damage evaluations are described elsewhere (Erlandsson et al, 1980, Nilsson et al,1982 In short, groups of 5 guinea pigs were kept in a circular wire-mesh cage and exposed simultaneously to noise directed from above. Pure-tones of two different frequencies were used as continuous steady-state stimuli.…”

Section: Methodsmentioning

confidence: 99%

“…It has been pointed out that one of the main factors constributing to the uncertainty in HTL measurements is the positioning of the earphones (Erlandsson et al, 1980). It is quite obvious that a more accurate way of defining the earphone position relative to the eardrum would be of great help in reducing the uncertainties in the HTL measurements.…”

Section: Uncertaintiesmentioning

confidence: 99%

“…below the critical level (Erlandsson, 1980). The implication of the difference in the slopes of the curves could be that different damage-mechanisms are in effect.…”

Section: I64mentioning

confidence: 99%

“…One can therefore expect that the rules of the game change at that point. Can this point, though, be characterized as a critical intensity (Price, 1981), a critical energy (Erlandsson et al, 1980;Nilsson et al, 1982), or a critical value of some other combination of intensity and time? Or, indeed, is the damage induced by supracritical exposures so capricious that we despair of ever finding the key to successful prediction?…”

Section: Animal Exposures: Total and Equal Energymentioning

confidence: 99%

“…(Ivarsson et al, 1980). Both audiometers were fitted with TDH-49 earphones, and in the first place with MX-41/AR cushions.…”

Section: Convertion Of Htl Values Obtained By Cushions To Specula Valmentioning

confidence: 99%

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Noise as a Public Health Problem: Proceedings of the International Congress (4th) Held at Turin (Italy) on June 21-25, 1983. Volume 1.

Rossi¹

1983

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Section: Methodsmentioning

confidence: 99%

Section: Uncertaintiesmentioning

confidence: 99%

“…below the critical level (Erlandsson, 1980). The implication of the difference in the slopes of the curves could be that different damage-mechanisms are in effect.…”

Section: I64mentioning

confidence: 99%

Section: Animal Exposures: Total and Equal Energymentioning

confidence: 99%

“…(Ivarsson et al, 1980). Both audiometers were fitted with TDH-49 earphones, and in the first place with MX-41/AR cushions.…”

Section: Convertion Of Htl Values Obtained By Cushions To Specula Valmentioning

confidence: 99%

See 3 more Smart Citations

Noise as a Public Health Problem: Proceedings of the International Congress (4th) Held at Turin (Italy) on June 21-25, 1983. Volume 1.

Rossi¹

1983

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The Effect of Impulse Noise on Cochlear Vessels

Vertes¹,

Axelsson²,

Hornstrand³

et al. 1984

Archives of Otolaryngology - Head and Neck Surgery

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and long-term changes in the cochlear vasculature and long-term changes in the sensorineuroepithelium were studied in guinea pigs after they were exposed to impulse noise. Vessel histology and cochlear hair cell loss were assessed, using a surface-preparation technique, and the results showed considerable variability. Hair cell loss and radial tears in the organ of Corti were a common finding in the animals killed four weeks after impulse-noise exposure. Impulse-noise exposure resulted in few cochlear vascular changes in the acutely and chronically affected groups. Compared with the results of our previous studies using continuous-noise exposure of different characteristics and in different mammals, this impulse-noise experiment resulted in a nonsignificant damaging effect on the cochlear vasculature. (Arch Otolaryngol 1984;110:111-115) Extensive speculations have been made concerning the traumatic mechanisms of noise on the cochlea. Among different theories to explain the sensorineural hearing loss at low¬ er sound intensities (ie, 85 to 120 dB measured on the A scale [dBA]), one proposal has been that deficient function of cochlear vessels leads to sensory cell loss. The concept is that sensory cells during increased need for oxygen and energy do not receive a sufficient supply from the cochlear vessels, possibly due to a vessel con¬ striction created by the noise itself. Most experimenters agree that me¬ chanical factors are responsible for damage to the sensorineuroep¬ ithelium at high sound intensities (ie, > 120 dBA). It is assumed that impulse-noise exposure results in tears of the cochlear membranes and other kinds of mechanical damage, eg, holes in the reticular lamina. Howev¬ er, there is little information avail¬ able concerning the specific shortterm persistent effects of impulse noise on cochlear vessels. In rats, ves¬ sel constriction in response to sound bursts can occur at intensities as low as at hearing threshold.1 Such vessel constriction in the periphery (ie, cochlea) could theoretically restrict the oxygen and energy supply and induce permanent sensory cell dam¬ age on a vascular basis. After expo¬ sure to gunshots, Kellerhals2 observed the packing of RBCs in the stria vascularis of experimental guinea pigs, which was not limited to the area of greatest hair cell damage. Stria vascularis capillaries were tightly packed with an abnormal homogenous mass of RBCs, but similar packing was absent in other vessels.These changes were present imme¬ diately and up to several days after exposure. Occlusion of lumina, col¬ lapse of vessels in the external wall of the cochlea, and degeneration of capil¬ laries with intravascular strands have been demonstrated with impulsenoise exposure.3 In animals exposed to sonic booms, hemorrhages were found in the scala tympani localized to the lower middle or basal turn of the cochlea." The mechanism was sup¬ posed to be a stretching of blood ves¬ sels on the tympanic surface of the basilar membrane, and the hemor¬ rhage was interpreted as a sign of mechanical dam...

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Local vs Systemic Effects of Acoustic Trauma on Cochlear Structure and Transport

Duvall

Robinson²

1987

Archives of Otolaryngology - Head and Neck Surgery

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\s=b\Whether certain effects of acoustic trauma on cochlear structure and function were due to local or systemic agents was investigated in the chinchilla. After unilateral ossicular disarticulation, the animals were given a noise exposure known to cause cochlear damage and vessel transport changes in the stria vascularis. The cochleas with disarticulated ossicular chains received an effective exposure well below one that causes pathologic damage. Only the cochleas with intact ossicular chains showed an increase in the permeability of the strial vessels to horseradish peroxidase tracer and manifested strial edema and organ of Corti damage. These results indicate that the effects of acoustic trauma on cochlear structure and strial vessel transport are induced locally, not systemically. In addition, the minimum time of exposure to 120-dB, 700-to 2800-Hz noise that causes massive cochlear damage in the chinchilla was shown to be between five and ten minutes. minutes or 120 dB for 22 minutes results in disruption and subsequent degeneration of the organ of Corti.1·2 In addition, edema of the stria vascu¬ laris develops several hours after the insult and persists for over five days. Preceding the appearance of strial edema and during its resolution, there is increased strial vessel permeability to the enzyme horseradish peroxidase (HRP). Yet, exposure to this noise at 111 dB or less for up to 22 minutes causes no discernible organ of Corti pathologic damage and only occasion¬ al strial edema.3 Changes in strial morphology after acoustic trauma may have several possible causes. Mechanical disrup¬ tion of the normal barrier between endolymph and perilymph permits intermixing of fluids that may, in turn, produce strial edema.4-7 This sequence of events is supported by the fact that strial edema follows mechanical rupture of Reissner's membrane5 or the organ of Corti.6 A second possibility is that altered strial morphology may represent a direct mechanical effect of the acoustic insult on the strial vessels themselves; this simple relation is implied by results recently reported by Ulehlova8 on guinea pigs exposed for 20 minutes or more to narrow-band noise at extremely high levels (142-dB SPL or higher) and then killed immediately.Third, it is possible that the strial edema is a result of systemic changes in the vascular tree; strial edema has been seen after obstruction of the cochlear venous system9 or following elevation of serum osmolality by means of osmotic diuretics.10·11 Final¬ ly, it may be the case that more than one of these possible mechanisms are involved; Shaddock et al7 have sug¬ gested, for example, that the direct effect of acoustic insult on the chin¬ chilla cochlea (in this case, impulse noise with peak levels of 160-dB SPL) may be exacerbated by the autonomie stress reaction of the vascular system to the trauma.To determine whether changes associated with acoustic trauma are due to local or systemic factors, one can compare the two ears from the same animal, one ear having been given an exposure that ...

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Hair Cell Damage In The Guinea Pig Due To Different Kinds Of Noise

Cited by 27 publications

References 40 publications

Noise as a Public Health Problem: Proceedings of the International Congress (4th) Held at Turin (Italy) on June 21-25, 1983. Volume 1.

Noise as a Public Health Problem: Proceedings of the International Congress (4th) Held at Turin (Italy) on June 21-25, 1983. Volume 1.

The Effect of Impulse Noise on Cochlear Vessels

Local vs Systemic Effects of Acoustic Trauma on Cochlear Structure and Transport

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