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

Abstract

\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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Cochlear Pericyte Responses to Acoustic Trauma and the Involvement of Hypoxia-Inducible Factor-1α and Vascular Endothelial Growth Factor

“…55 Increased expression of desmin protein may be an adaptive strategy for coping with the physiological challenges imposed by loud sound. Higher internal pressure in capillaries may require more pericyte coverage to maintain vascular integrity.…”

A critical evaluation of “leakage” at the cochlear blood-stria-barrier and its functional significance

“…The acute effects of noise exposure on the stria have been characterized by a number of authors over decades. An acute increase in strial capillary permeability is supported by several studies (e.g., Duvall et al, 1974 ; Hukee and Duvall, 1985 ; Duvall and Robinson, 1987 ; Goldwyn and Quirk, 1997 ; Suzuki et al, 2002 ; Shi, 2009a , b ; Hou et al, 2018 ; Jiang et al, 2023 ). Most of these reports are consistent with the idea that the increase in permeability was due to an increase in transcellular transport (but see Wu et al, 2014 ).…”