Sound-induced cochlear ischemia/hypoxia as a mechanism of hearing loss
Alfred L Nuttall
Department of Otolaryngology, NRC04, Oregon Health Sciences University, Portland, Oregon, USA and Kresge Hearing Research Institute, University of Michigan, Ann Arbor, MI 97201-3098, USA
This review will briefly examine evidence supporting the hypothesis that sound causes changes in cochlear blood flow, intracochlear oxygen levels, and the morphology of cochlear blood vessels. A survey of the literature shows that traditional histopathological studies provided such evidence and that decreased cochlear blood flow can be demonstrated and measured by laser Doppler flowmetry and by direct observation of cochlear microvessels. Oxygen levels also decline and possibly to a greater degree than blood flow. There is also evidence that in certain circumstances sound can increase blood flow.
Reduced blood flow, or reduced oxygenation, is critically important in an organ system with high energy needs like the cochlea. Therefore, a second hypothesis, that sound-induced reduction in CBF represents a functional ischemia, will be explored in examining the relevance of traditional ischemia/reperfusion models to cochlear damage. It is found that reactive oxygen species (free radicals and oxidizing ions) are present in sound-induced hearing loss and thus there is evidence that an ischemia/reperfusion type of injury occurs during loud sound exposures.
Alfred L Nuttall
Oregon Hearing Research Centre, NRC04, Department of Otolaryngology/Head & Neck Surgery, Oregon Health Sciences University, 3181 S.W. Sam Jackson Park Rd., Portland, OR 97201-3098
|How to cite this article:|
Nuttall AL. Sound-induced cochlear ischemia/hypoxia as a mechanism of hearing loss.Noise Health 1999;2:17-31
|How to cite this URL:|
Nuttall AL. Sound-induced cochlear ischemia/hypoxia as a mechanism of hearing loss. Noise Health [serial online] 1999 [cited 2021 Dec 7 ];2:17-31
Available from: https://www.noiseandhealth.org/article.asp?issn=1463-1741;year=1999;volume=2;issue=5;spage=17;epage=31;aulast=Nuttall;type=0