The effects of noise on histological measures of the cochlear vasculature and red blood cells: A review

Axelsson, A.; Dengerink, H. A.

doi:10.1016/0378-5955(87)90125-0

Cited by 54 publications

(25 citation statements)

References 12 publications

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“…Numerous histological and in vivo studies performed under a number of different exper imental conditions have concluded that there are only few consistent vascular changes [see reviews in [4][5][6][7][8][9][10]. Instead, it has been suggest ed that changes in CoBF are an epiphenomenon, secondary to physiological adjustments resulting from the noise stress [4].…”

Section: Discussionmentioning

confidence: 99%

“…However, a close temporal relationship between changes in CoBF and endolymphatic or perilymphatic partial pressure of oxygen (pCF) has not yet been demonstrated with acoustic overstimu lation. CoBF has been evaluated in a number of species subjected to noise using different exposure parameters and observation times [sec reviews in [4][5][6][7][8][9][10]. It has concluded that there arc no uniform reproducible morpho logical changes in the cochlear vessels and no defined thresholds for a change in CoBF in vivo after exposure to pure tones of various frequencies, octave, narrow or broad-band noise and impulse noise.…”

mentioning

confidence: 99%

“…In tro d u ctio n Development of noise-induced hearing loss is a function of exposure parameters, rest periods, species and individual condition [for recent reviews, see [1][2][3][4]. Noise-induced alter ations in cochlear blood flow (CoBF) have been suggested as a causative factor leading to cochlear hypoxia, morphological damage and hearing loss [see reviews in [4][5][6][7][8][9][10]. However, a close temporal relationship between changes in CoBF and endolymphatic or perilymphatic partial pressure of oxygen (pCF) has not yet been demonstrated with acoustic overstimu lation.…”

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confidence: 99%

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Noise-Induced Cochlear Hypoxia Is Intensity Dependent, Correlates with Hearing Loss and Precedes Reduction of Cochlear Blood Flow

Lamm

Arnold²

1996

Audiol Neurotol

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Anesthetized and artificially ventilated guinea pigs were exposed to broad-band noise of 95, 101, 106 or 115 dB SPL for 30 min and studied for 180 min after cessation of noise. The partial pressure of oxygen (pO₂) in the perilymph, the cochlear blood flow (CoBF) and auditory-evoked potentials were continuously recorded. Arterial blood pressure, electrocardiogram, inspiratory and expiratory gas levels, arterial blood gas levels and acid-base status were kept stable to exclude influences of these parameters on cochlear parameters. Exposure to 95 dB SPL did not affect perilymphatic pO₂or CoBF. Cochlear microphonics (CMs) were reduced, but compound action potentials of the auditory nerve (CAPs) and auditory brainstem potentials (ABRs) increased after exposure to this low-level noise. Perilymphatic pO₂decreased during exposure to 101 dB SPL and then further decreased during the subsequent 60 min after cessation of the noise. CoBF did not change significantly during and 30 min after noise but then paralleled the decline of perilymphatic pO₂ However, both parameters showed a clear indication of recovery in the sec-ond and third hours after noise. At 101 dB SPL, CMs were again reduced immediately, CAPs were unaltered and ABRs again increased. Exposure to 106 and to 115 dB SPL resulted in a decrease in both perilymphatic pO₂and CoBF; this decrease began during the exposure but became progressively worse after the noise. Hearing loss was observed immediately with exposure and showed no signs of further deterioration after cessation. The observed time courses of changes are important. They reveal that hearing loss and cochlear hypoxia precede reduction in CoBF due to noise exposure. The potential mechanisms underlying these effects are discussed.

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Section: Discussionmentioning

confidence: 99%

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confidence: 99%

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Noise-Induced Cochlear Hypoxia Is Intensity Dependent, Correlates with Hearing Loss and Precedes Reduction of Cochlear Blood Flow

Lamm

Arnold²

1996

Audiol Neurotol

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“…Identification of this safe and effective antioxidant intervention that attenuates NIHL provides a compelling rationale for human trials in which free radical scavengers are used to eliminate this single major cause of acquired hearing loss. Keywords cochlea; free radical; noise; hearing; antioxidant; vasodilation Mechanical destruction of cells in the organ of Corti was once assumed to be the primary cause of noise-induced hearing loss (NIHL) [1][2][3][4][5][6][7][8], with perhaps some effect of reduced blood flow to the inner ear [9][10][11][12][13][14][15][16][17][18]. We now know that another key factor is intense metabolic activity that results in production of excess free radicals [19][20][21][22][23] and lipid peroxidation products [24].…”

Section: Introductionmentioning

confidence: 99%

Free radical scavengers vitamins A, C, and E plus magnesium reduce noise trauma

Prell

Hughes

Miller

2007

Free Radical Biology and Medicine

201

188

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Free radical formation in the cochlea plays a key role in the development of noise-induced hearing loss (NIHL). The amount, distribution, and time course of free radical formation have been defined, including a clinically significant formation of both reactive oxygen species and reactive nitrogen species 7-10 days following noise exposure. Reduction in cochlear blood flow as a result of free radical formation has also been described. Here we report that the antioxidant agents, vitamins A, C, and E, act in synergy with magnesium to effectively prevent noise-induced trauma. Neither the antioxidant agents nor magnesium reliably reduced NIHL or sensory cell death with the doses we used when these agents were delivered alone. In combination, however, they were highly effective in reducing both hearing loss and cell death even with treatment initiated just one hour prior to noise exposure. This study supports roles for both free radical formation and noise-induced vasoconstriction in the onset and progression of NIHL. Identification of this safe and effective antioxidant intervention that attenuates NIHL provides a compelling rationale for human trials in which free radical scavengers are used to eliminate this single major cause of acquired hearing loss. Keywords cochlea; free radical; noise; hearing; antioxidant; vasodilation Mechanical destruction of cells in the organ of Corti was once assumed to be the primary cause of noise-induced hearing loss (NIHL) [1][2][3][4][5][6][7][8], with perhaps some effect of reduced blood flow to the inner ear [9][10][11][12][13][14][15][16][17][18]. We now know that another key factor is intense metabolic activity that results in production of excess free radicals [19][20][21][22][23] and lipid peroxidation products [24]. Noise-induced production of reactive oxygen species (ROS) in the cochlea has now been well characterized, and several recent reviews are available [25][26][27]. Mitochodrial dysfunction and ROS production have been implicated in numerous neurodegenerative syndromes and diseases [28-34, see 35,36]. The use of antioxidant agents holds significant therapeutic promise for many neurodegenerative processes [32,33,[37][38][39][40][41][42], and there is some suggestion that Correspondence to: C. G. Le Prell, Kresge Hearing Research Institute, University of Michigan, 1301 East Ann Street, Ann Arbor, MI 48109-0506, USA. Tel: +1-734-763-5104; fax +1-734-764-0014. E-mail address: colleeng@umich.edu. Disclosure. Dr. Miller is a founding member and Chairman of the Board of Directors at OtoMedicine, Inc., a company that has an option to license the intellectual property described in this report. Dr. Le Prell is a paid consultant to OtoMedicine, Inc. Drs. Miller and Le Prell have disclosed these relationships to the Medical School Conflict of Interest Board at the University of Michigan; conflict management plans including semi-annual review by the Board are in place.Publisher's Disclaimer: This is a PDF file of an unedited manuscript that has been accepted for publicatio...

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“…Until a decade ago, the prevailing view of NIHL was that it was caused by mechanical destruction of the delicate membranes of the hair cells and supporting structures of the organ of Corti (Spoendlin, 1971;Elliott, 1972,1973;Hunter-Duvar and Bredberg, 1974;Hawkins et al, 1976;Mulroy et al, 1998), with perhaps some effect of intense noise on blood flow to the inner ear (Perlman and Kimura, 1962;Hawkins, 1971;Hawkins et al, 1972;Lipscomb and Roettger, 1973;Santi and Duvall, 1978;Axelsson and Vertes, 1981;Axelsson and Dengerink, 1987;Duvall and Robinson, 1987;Scheibe et al, 1993;Miller et al, 1996). We now know another significant factor is intense metabolic activity, which increases mitochondrial free radical formation.…”

Section: Noise-induced Rosmentioning

confidence: 99%

Mechanisms of noise-induced hearing loss indicate multiple methods of prevention

et al. 2007

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Recent research has shown the essential role of reduced blood flow and free radical formation in the cochlea in noise-induced hearing loss (NIHL). The amount, distribution, and time course of free radical formation have been defined, including a clinically significant late formation 7-10 days following noise exposure, and one mechanism underlying noise-induced reduction in cochlear blood flow has finally been identified. These new insights have led to the formulation of new hypotheses regarding the molecular mechanisms of NIHL; and, from these, we have identified interventions that prevent NIHL, even with treatment onset delayed up to 3 days post-noise. It is essential to now assess the additive effects of agents intervening at different points in the cell death pathway to optimize treatment efficacy. Finding safe and effective interventions that attenuate NIHL will provide a compelling scientific rationale to justify human trials to eliminate this single major cause of acquired hearing loss.

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The effects of noise on histological measures of the cochlear vasculature and red blood cells: A review

Cited by 54 publications

References 12 publications

Noise-Induced Cochlear Hypoxia Is Intensity Dependent, Correlates with Hearing Loss and Precedes Reduction of Cochlear Blood Flow

Noise-Induced Cochlear Hypoxia Is Intensity Dependent, Correlates with Hearing Loss and Precedes Reduction of Cochlear Blood Flow

Free radical scavengers vitamins A, C, and E plus magnesium reduce noise trauma

Mechanisms of noise-induced hearing loss indicate multiple methods of prevention

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