TY - JOUR
T1 - Effects of carbon monoxide on cochlear electrophysiology and blood flow
AU - Fechter, Laurence D.
AU - Thorne, Peter R.
AU - Nuttall, Alfred L.
N1 - Funding Information:
The authors wish to acknowledget he skillful technicaal ssistancoef Nadine Brown and Michelle Griffiths in conductingt hesee xperimentso, f the ECMO laboratory and staff at the University of Michigan Medical Center for providing accesst o theirb lood gasa nalysisla b and to ProfessorJ oseph Hawkins,J r. for his helpfulc ommentso n an earlier draft of this manuscriptT. his work was supported in part by PHS grantsE S-02852R, CDA ES-00125 for L.F., USPHS InternationalR esearchF ellow-ship TWO3473f or P.T., and NIH NS11731 for A.N.
PY - 1987
Y1 - 1987
N2 - The belief that the cochlea is particularly vulnerable to a reduction in oxygen availability comes predominantly from studies reporting the disruption of electrophysiological measures, such as the compound action potential, endocochlear potential, inner hair cell intracellular potentials or afferent nerve fiber responses by asphyxiation. Because hypoxia has frequently been suggested as an underlying mechanism by which many ototoxic agents produce injury, and because such agents are not likely to completely disrupt oxygen delivery, we investigated the effects of graded hypoxia (using doses of carbon monoxide) on cochlear blood flow, the compound action potential (CAP) and the cochlear microphonic (CM). High doses of carbon monoxide injected intra-peritoneally yielded reversible loss of the CAP sensitivity for high frequency tone bursts, the extent of which was dose dependent. The loss was observed first at the highest frequency tested (50 kHz) and as carboxyhemoglobin levels increased, contiguous lower frequencies were influenced. Recovery progressed from low to high frequencies as carboxyhemoglobin levels declined. Carbon monoxide administration also produced a dose dependent elevation in the cochlear blood flow measured by a laser Doppler flow monitor. The data suggest that carbon monoxide administration disrupts cochlear function only under extremely severe exposure conditions. An elevation in cochlear blood flow may well serve as a protective mechanism which maintains cochlear function in the face of declining blood oxygen carrying capacity and delivery. While the site of action of carbon monoxide in the cochlea is uncertain, the data clearly indicate that elements involved in the generation of the CAP for high frequency tones are particularly vulnerable. This suggests that such elements may have different metabolic requirements from other lower frequency regions of the cochlea and/or that oxygen delivery (blood circulation) differs in the basal portion of the cochlea.
AB - The belief that the cochlea is particularly vulnerable to a reduction in oxygen availability comes predominantly from studies reporting the disruption of electrophysiological measures, such as the compound action potential, endocochlear potential, inner hair cell intracellular potentials or afferent nerve fiber responses by asphyxiation. Because hypoxia has frequently been suggested as an underlying mechanism by which many ototoxic agents produce injury, and because such agents are not likely to completely disrupt oxygen delivery, we investigated the effects of graded hypoxia (using doses of carbon monoxide) on cochlear blood flow, the compound action potential (CAP) and the cochlear microphonic (CM). High doses of carbon monoxide injected intra-peritoneally yielded reversible loss of the CAP sensitivity for high frequency tone bursts, the extent of which was dose dependent. The loss was observed first at the highest frequency tested (50 kHz) and as carboxyhemoglobin levels increased, contiguous lower frequencies were influenced. Recovery progressed from low to high frequencies as carboxyhemoglobin levels declined. Carbon monoxide administration also produced a dose dependent elevation in the cochlear blood flow measured by a laser Doppler flow monitor. The data suggest that carbon monoxide administration disrupts cochlear function only under extremely severe exposure conditions. An elevation in cochlear blood flow may well serve as a protective mechanism which maintains cochlear function in the face of declining blood oxygen carrying capacity and delivery. While the site of action of carbon monoxide in the cochlea is uncertain, the data clearly indicate that elements involved in the generation of the CAP for high frequency tones are particularly vulnerable. This suggests that such elements may have different metabolic requirements from other lower frequency regions of the cochlea and/or that oxygen delivery (blood circulation) differs in the basal portion of the cochlea.
KW - Carbon monoxide hypoxia
KW - Cochlear blood flow
KW - Cochlear microphonic
KW - Compound action potential
KW - Laser Doppler
KW - Ototoxicity
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U2 - 10.1016/0378-5955(87)90024-4
DO - 10.1016/0378-5955(87)90024-4
M3 - Article
C2 - 3583935
AN - SCOPUS:0023277169
SN - 0378-5955
VL - 27
SP - 37
EP - 45
JO - Hearing Research
JF - Hearing Research
IS - 1
ER -