The effect of nitrogen mustard-N-oxide (Nitromin®) upon the click evoked N1 latency was examined in 14 albino guinea pigs. Various dosage of Nitromin® ranged from 5 to 30 mg/kg were given intravenously and the cochlear potentials were recorded 3 to 7 days after the administration. The animals were histologically examined with a surface preparation technique after the measurements. In all animals except one, the thresholds of AP to the filtered tone burst were elevated especially in high frequency range. In addition to the amplitude reduction, the N1 latency evoked by a click was prolonged in 12 animals. Narrow-band analysis of the N1 revealed that the latency was equally prolonged in all frequencies, although the amount of the amplitude reduction was much larger in high frequency. The histological examination exhibited the various degrees of the outer hair cell damage and the results obtained in electrophysiological studies were correlated with these findings. It was concluded that the prolongation of the Ni latency in Nitromin® treated animals was due to the dysfunction of outer hair cells along the entire cochlear partition.
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