This study examined the effects of acoustic exposure at different intensities on cochlear blood flow (CBF) using laser Doppler flowmetry. CBF was measured in anesthetized guinea pigs exposed to either a 10 kHz pure tone at 125, 105, or 90 dB SPL, or wide-band noise at 85 dB SPL for 1 h. Mean arterial blood pressure and heart rate were recorded continuously. Arterial acid-base status, cochlear temperature, cochlear microphonics (CM), and compound action potentials (CAP) were measured before and after exposure. There was a small, but significant, steady decline in basal CBF after 40 min loud sound exposure (125 dB SPL), but no change in basal CBF occurred with the lower intensities (85-105 dB SPL). In contrast, there was a significant increase in apical CBF after 1 h exposure to either moderate wideband noise (85 dB SPL) or a 10 kHz tone at 105 dB SPL. These changes persisted during a 20-min post-exposure period. In most cases, the cochlear temperature and cardiorespiratory variables monitored remained unchanged during and after the exposures as compared to the controls. CM and CAP amplitudes showed extensive losses after acoustic overstimulation (125 dB SPL), but no permanent changes were found at the lower intensities used. The present findings confirm the occurrence of intensity-related effects of acoustic exposure on the cochlear microcirculation.

The effect of magnesium (Mg) on noise-induced hearing loss was investigated in two groups of adult pigmented guinea pigs maintained either on optimal or suboptimal (physiologically high or low) Mg produced by different diets. The total Mg concentrations of the perilymph (PL), cerebrospinal fluid, blood plasma and red blood cells were measured by atomic absorption spectrometry and were found to differ significantly between the two groups (P < 0.01). One ear of each animal was exposed to either a single shooting impulse at a peak pressure level of 187 dB or two impulse noise series at a rate of 1/s and peak pressure levels of 150 dB (1,000 impulses) and 167 dB (2,280 impulses), respectively. Temporary (TTS) and permanent (PTS) hearing threshold shifts in anesthetized animals were measured 2 h and 1 week after the noise exposure, using auditory brain stem response (ABR) audiometry at a frequency range from 3.75 to 30 kHz. Exposure to the single noise impulse resulted in a mean TTS that was significantly lower in the high Mg group than that in the low Mg group (P < 0.05), although no substantial PTS was observed in either group. In the animals exposed to 150 dB noise, the TTS showed a tendency towards an Mg-related reduction at the higher frequencies. A small difference in PTS was found between the low Mg and high Mg groups, but was not significant. Exposure to the 167-dB noise series caused a considerable TTS, which was significantly lower in the high Mg group at 7.5 and 15 kHz than in the low Mg group (P < 0.05). The mean PTS showed a significant difference between the two Mg groups over the whole frequency range (P < 0.05) and was found to correlate negatively with the total Mg concentrations of both PL and plasma (P < 0.05). Moreover, the high Mg group showed a faster recovery from the hearing threshold shift than the low Mg group. The present findings show that preventive oral Mg supplements can significantly reduce the rate of acoustic trauma caused by high-level impulse noise exposure in the guinea pig.

Changes in cochlear microcirculation and oxygenation and auditory function were examined in anesthetized guinea pigs during prolonged hypoxic ventilation (8% oxygen in nitrogen) for 1 h. Cochlear blood flow and perilymphatic oxygen partial pressure were measured using laser Doppler flowmetry and oxygen-sensitive microelectrodes. Auditory function was examined by recording cochlear microphonics, compound action potentials and auditory evoked brainstem response. Blood pressure and heart rate were monitored. During systemic hypoxia, the perilymphatic PO2 dropped on average to about 70% of the initial value. Cochlear and brainstem potentials showed a mean reduction to 75-82%. Different effects of hypoxia on cochlear blood flow were observed and included decreases as well as increases. Mean arterial blood pressure declined significantly during hypoxia, while the heart rate remained constant. The changed variables returned to normal during reventilation with room air. The findings are discussed with regard to their significance as an animal model for the study of hypoxia-induced cochlear pathophysiology.