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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