Disruption of Cochlear Potentials by Chemical Asphyxiants: Cyanide and Carbon Monoxide

Details

• Personal Author:
  Chen G-D ; Fechter LD ; Tawackoli W
• Description:
  While ischemia, hypoxic hypoxia, and carbon monoxide (CO) have received extensive study designed to characterize mechanisms by which they disrupt cochlear function, little data are available concerning cyanide's potential to disrupt auditory function. In this study, disruption of the compound action potential (CAP) and endocochlear potential (EP) by cyanide and CO was compared in rats treated with potassium cyanide (KCN) (7 mg/kg ip), saline, CO (35 ml/kg ip), and air. Acute KCN administration significantly suppressed CAP and EP transiently. The effect was seen initially on EP with CAP impairment occurring a few minutes later. Acute CO injection also suppressed the CAP significantly, but the effect was far smaller, occurred later in time, and lasted longer than the effect of KCN. The effect of CO on EP was equivocal. There was a good correspondence between blood cyanide levels and impairment of cochlear function; carboxyhemoglobin (HbCO) levels were elevated during the period when cochlear function was impaired, but recovery of cochlear function preceded the return of normal oxyhemoglobin. Both KCN and CO had somewhat preferential effects on high-frequency tones. Repeated cyanide administration caused a persistent CAP threshold elevation despite the rapid recovery of EP and CAP observed following acute KCN administration. The data suggest that acute KCN administration has a prominent disruptive effect at the stria vascularis presumably by disrupting the electron transport chain in this metabolically active structure. The principal target for acute CO ototoxicity in the cochlea is probably not the stria vascularis. [Description provided by NIOSH]
• Subjects:
  Animals Carbon Monoxide Cyanides Lung Lung Diseases Noise Noise, Occupational Occupational Health Respiratory System Respiratory Tract Diseases Safety

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• Keywords:
  Animal Studies Auditory System Auditory Threshold Author Keywords: Cyanide Carbon Monoxide Cochlea Exposure Assessment Hypoxia Noise Exposure Ototoxicity Rat

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• ISSN:
  0892-0362
• Document Type:
  Text
• Funding:
  Grant
• Genre:
  Journal Article
• Place as Subject:
  Oklahoma ; OSHA Region 6
• CIO:
  National Institute for Occupational Safety and Health (NIOSH)
• Topic:
  Workplace Safety & Health
• Location:
  North America
• Pages in Document:
  157-165
• Volume:
  23
• Issue:
  2
• NIOSHTIC Number:
  nn:20057889
• Citation:
  Neurotoxicol Teratol 2001 Mar-Apr; 23(2):157-165
• Contact Point Address:
  Laurence D Fechter, Oklahoma Center for Toxicology, College of Pharmacy, University of Oklahoma Health Sciences Center, 1110 North Stonewall Street, PO Box 26901, Oklahoma City, OK 73190, USA
• Email:
  fechter@ouhsc.edu
• CAS Registry Number:
  Carbon monoxide (CAS RN 630-08-0)
• Federal Fiscal Year:
  2001
• NORA Priority Area:
  Disease and Injury: Hearing Loss
• Performing Organization:
  University of Oklahoma, Health Sciences Center, Oklahoma Center for Toxicology, Oklahoma City, Oklahoma
• Peer Reviewed:
  True
• Start Date:
  19970901
• Source Full Name:
  Neurotoxicology and Teratology
• End Date:
  20000831
• Collection(s):
  National Institute for Occupational Safety and Health
• Main Document Checksum:
  urn:sha-512:9c86fb281bca7005fd3bd2878bf838cf707f054d089ece830755194f16c58fcd9e2d688b4c55d6590c1eae15a0f4d94b387ef4d3dfa91b9d129336a0cea38062
• Download URL:
  https://stacks.cdc.gov/view/cdc/215095/cdc_215095_DS1.pdf
• File Type:
  [PDF - 180.87 KB ]