Cochlear Blood Flow in Acoustic Trauma

Perlman, H. B.; Kimura, Robert S.

doi:10.3109/00016486209126927

Cited by 118 publications

(31 citation statements)

References 12 publications

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“…Daily treatment that continued through day 5 post-noise presumably reduced the late forming radicals revealed in the studies of Yamashita et al [86]. Unlike most tissues, where increased metabolism increases blood flow to provide additional oxygen to stressed cells, reduced blood vessel diameter and red blood cell velocity [97,98] and decreased blood flow [9,10,16,26,99] are observed in the cochlea post-noise. This noise-induced vasoconstriction is a direct consequence of noise-induced formation of 8-isoprostane-F 2α , a vasoactive by-product of free radicals [46], and thus, antioxidant agents that reduce free radical formation may eliminate noise-induced vasoconstriction.…”

Section: Mechanism Of Actionmentioning

confidence: 98%

“…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%

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

Prell

Hughes

Miller

2007

Free Radical Biology and Medicine

198

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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Section: Mechanism Of Actionmentioning

confidence: 98%

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

198

188

View full text Add to dashboard Cite

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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%

“…However, in the cochlea, high levels of noise decrease blood flow (Perlman and Kimura, 1962;Lipscomb and Roettger, 1973;Thorne and Nuttall, 1987;Miller et al, 1996;2006b). Decreased blood flow in the cochlea is a direct consequence of noise-induced reductions in blood vessel diameter and red blood cell velocity (Quirk et al, 1992;Quirk and Seidman, 1995).…”

Section: Vasodilation and Nihlmentioning

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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“…2) (24). The decrease in oxygen tension in the endolymph occurring with acoustic stimulation (25,26) must reflect an increase in the rate of oxygen utilization by the cochlea to the point that utilization outstrips supply.…”

Section: Noise-induced Ototoxicitymentioning

confidence: 99%