[abstract] Sound Conditioning and Cerebral Oxygen Toxicity

Abstract

Background: The pathogenesis of cerebral oxygen toxicity (COT), is related to high levels of reactive oxygen species (ROS) overcoming the body's antioxidant mechanisms, leading to lipid, protein and nucleic acid peroxidation. Noise-induced hearing loss (NIHL) has been shown to result from ischemia-reperfusion, in which ROS play a major role. Sound conditioning prevented NIHL in various animal species, and was associated with significant elevation of the antioxidant enzymes measured in the inner ear. In this study the hypothesis that sound conditioning attenuates COT was tested. Materials and Methods: Hearing thresholds of 8 male Sprague-Dawley rats (250-300 g) were estimated using Auditory Brainstem Evoked Potentials (ABEP) under general anesthesia, with core temperature maintained at approximately 37OC. Sound conditioning was carried out by exposure to 95 dB SPL, 4kHz centered, free field noise for 72 hours. Oxygen exposure at 6 ATA was monitored by continuous EEG recording, and the latency to the first electrical discharge immediately preceding the appearance of seizures was measured. Hearing threshold and latency to EEG discharge under 6 ATA oxygen before and after exposure to the sound conditioning protocol were compared. Results: Average baseline hearing threshold was 19+/-17 dB HL pre-, and 33+/-16 dB HL post-sound exposure (p=0.006). The average latency to COT was 17.8+/-6.2 and 14.5+/-3.7 minutes, respectively. The latter were not significantly different. No significant correlation was found between hearing threshold shift and latency to COT. Conclusions: Sound conditioning did not modify COT. The repeated oxygen exposure design may have masked possible sound conditioning effects on COT.