Acute acoustic trauma (AAT) is a sudden sensorineural hearing loss caused by exposure of the hearing organ to acoustic overstimulation, typically an intense sound impulse, hyperbaric oxygen therapy (HOT), which favors repair of the microcirculation, can be potentially used to treat it. Hence, this study aimed to assess the effects of HOT on guinea pigs exposed to acoustic trauma. Fifteen guinea pigs were exposed to noise in the 4-kHz range with intensity of 110 dB sound level pressure for 72 h. They were assessed by brainstem auditory evoked potential (BAEP) and by distortion product otoacoustic emission (DPOAE) before and after exposure and after HOT at 2.0 absolute atmospheres for 1 h. The cochleae were then analyzed using scanning electron microscopy (SEM). There was a statistically significant difference in the signal-to-noise ratio of the DPOAE amplitudes for the 1- to 4-kHz frequencies and the SEM findings revealed damaged outer hair cells (OHC) after exposure to noise, with recovery after HOT (p = 0.0159), which did not occur on thresholds and amplitudes to BAEP (p = 0.1593). The electrophysiological BAEP data did not demonstrate effectiveness of HOT against AAT damage. However, there was improvement of the anatomical pattern of damage detected by SEM, with a significant reduction of the number of injured cochlear OHC and their functionality detected by DPOAE.

Auditory conditioning consists of the pre-exposure to low levels of a potential harmful agent to protect against a subsequent harmful presentation. The agent that was first tested was noise. This paradigm was more recently successfully tested with other agents. Nonetheless, the vast majority of the studies utilize the same agent to condition and to cause the trauma. The aim of this study was to verify whether conditioning with an agent different from the agent used to cause the trauma can also be effective. Thus, the following groups were organized: group Cont, which is the noise trauma control group, was exposed to 110-dB broadband noise centered at 4 kHz for 72 h; group Gent, which is the gentamicin conditioning control group, was administered 30 mg/kg of gentamicin daily for 30 consecutive days; and group Expt was conditioned with gentamicin similarly to group Gent and then subjected to a noise trauma similarly to group Cont. The animals were functionally and morphologically evaluated through the measurement of the auditory brainstem response and scanning electron microscopy, respectively. The following variables were investigated: outer hair cell injury and auditory threshold shift. The group that was conditioned with the drug exhibited significantly less outer hair cell damage, 10.8 and 22.9%, respectively (p = 0.0146), although did not maintain the proper functioning of the auditory system. We, therefore, conclude that conditioning with a different agent from that used to cause the trauma is effective, which suggests that both agents that were used promote similar mechanisms of self-protection.

Conditioning with 85 dB broadband noises, 30 min a day for ten consecutive days does not protect against an ototoxic gentamicin administration of 160 mg/kg/day for ten consecutive days in the guinea pig.

COLOMBARI, G. C. Otoprotection against acoustic trauma: Effects of hyperbaric oxygen therapy and corticoid. 2011. 80 f.