TY - JOUR
T1 - Electrically stimulated increases in cochlear blood flow
T2 - II. Evidence of neural mediation
AU - Sillman, J. S.
AU - Masta, R. I.
AU - LaRouere, M. J.
AU - Nuttall, A. L.
AU - Miller, J. M.
PY - 1989
Y1 - 1989
N2 - In a companion paper, we reported that electrical stimulation increased cochlear blood flow (CBF). This response was found to be an increasing function of current intensity and was frequency-selective, with the best response at approximately 500 Hz continuous sinusoidal current. The present investigation seeks to discover the mechanism of this effect. Direct measurement of cochlear temperature during electrical stimulation revealed no evidence of local heating. Autonomic neuronal activation is not likely, as neither atropine, hexamethonium, nor propranolol abolished the evoked CBF response. Strial activity could be suppressed by the use of furosemide, but the evoked CBF response persisted. Inactivation of auditory afferent neurons with kainic acid also did not change the evoked CBF response. Dimethyl sulfoxide, a potent oxygen-free radical scavenger, did suppress the evoked CBF response to a small but significant degree. This suggests that oxygen-free radicals may be produced within the cochlea during electrical stimulation. Finally, the evoked CBF response was completely suppressed by procaine and tetrodotoxin, with recovery of evoked CBF response accompanying recovery of cochlear action potentials. These data indicate that stimulation of neural fibers, distinct from autonomic and auditory afferent neurons, may modulate CBF.
AB - In a companion paper, we reported that electrical stimulation increased cochlear blood flow (CBF). This response was found to be an increasing function of current intensity and was frequency-selective, with the best response at approximately 500 Hz continuous sinusoidal current. The present investigation seeks to discover the mechanism of this effect. Direct measurement of cochlear temperature during electrical stimulation revealed no evidence of local heating. Autonomic neuronal activation is not likely, as neither atropine, hexamethonium, nor propranolol abolished the evoked CBF response. Strial activity could be suppressed by the use of furosemide, but the evoked CBF response persisted. Inactivation of auditory afferent neurons with kainic acid also did not change the evoked CBF response. Dimethyl sulfoxide, a potent oxygen-free radical scavenger, did suppress the evoked CBF response to a small but significant degree. This suggests that oxygen-free radicals may be produced within the cochlea during electrical stimulation. Finally, the evoked CBF response was completely suppressed by procaine and tetrodotoxin, with recovery of evoked CBF response accompanying recovery of cochlear action potentials. These data indicate that stimulation of neural fibers, distinct from autonomic and auditory afferent neurons, may modulate CBF.
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U2 - 10.1177/019459988910100310
DO - 10.1177/019459988910100310
M3 - Article
C2 - 2508007
AN - SCOPUS:0024432351
SN - 0194-5998
VL - 101
SP - 362
EP - 374
JO - Otolaryngology - Head and Neck Surgery
JF - Otolaryngology - Head and Neck Surgery
IS - 3
ER -