Effect of 2.1 MPa and 4.1 MPa H2O2 exposure on auditory brain stem evoked potential in mice.

Brain auditory evoked potential (BAEP) in mice exposed to hyperbaric H2O2 pressure was monitored to reveal the correlation between altered synaptic transmission and hydrogen narcosis or isobaric HPNS. Inter peak latencies and wave amplitudes were selected as indices of assessment. The animals were exposed either to He-O2 or H2-O2 at 2.1 MPa and 4.1 MPa. Results showed that synaptic transmission was inhibited to various extents. The inhibition was partly due to the narcotic effect of hydrogen, which was added to the effect caused by hydrostatic pressure. On the other hand, asymmetrical reaction of each segment in the neuro-network might be responsible for the occurrence of HPNS.

Changes in human brainstem auditory evoked potentials during a 1,100 kPa He-O2 simulated saturation dive.

Four divers were chosen as subjects to conduct the 1,100 kPa He-O2 simulated saturation dive. Brainstem auditory evoked potentials of the divers were monitored during different stages of the exposure. At 1,100 kPa, with both 10 and 50 Hz clicks, interpeak latencies I-V were prolonged by 0.242 and 0.360 ms, respectively, indicating impedance of synaptic transmission. Results showed that interpeak latencies I-V were prolonged by 0.242 and 0.360 ms, respectively, indicating impedance of synaptic transmission. However, the latency of wave I was shortened by 0.11 ms, which was presumed to be due to different mechanical sound transmission velocity at hyperbaric helium environment. Interestingly, the latency of wave I prolonged gradually during hyperbaric exposure to 1,100 kPa. This might be used for the measurement of effects of hydrostatic pressure and He on the central nervous system (CNS). These changes coupled with easy perspiration and fatigue of the divers suggest that the pressure of the present experiment had certain effects of the CNS on the divers, although they were moderate and temporary.