By measuring potential drop produced by a constant current across the partition between scala media and scala tympani the average resistance of this partition was found to be 4700 ohms at the round window, 3500 ohms at the first turn, 1200 ohms at the second turn and 600 ohms at the third turn. Just preceding or simultaneously with a drop in d.c. potential there was a drop in resistance in response to loud sound. Recovery of the resistance preceded recovery of d.c. potential. Anoxia first lowered d.c. potential, then resistance. Both appeared to recover at nearly the same time. Destruction of the fourth, third and second cochlear turns did not affect d.c. potential or microphonics in scala media recorded from the first turn through the round window. Both were abolished upon destruction of the first turn. No spread of current was found from one turn to another. Implications of these results are discussed.
In order to evaluate the role played by endolymphatic hypoxia on deafness due to exposure to loud sounds, continuous recordings of oxygen availability, action potential, and microphonics were taken during asphyxia, "chronic hypoxia," and after loud sounds. The curves so obtained are compared and show that hypoxia may play an important contributory role in the temporary losses of hearing following loud sounds. Possible mechanisms of auditory trauma are reviewed briefly.
Using a potassium chloride reference microelectrode and an antimony-Cerroseal alloy active microelectrode, the pH of the perilymph exposed to the atmosphere was found to be 7.8–8.0 and the endolymph in situ 7.3–7.5 in the guinea pig. The acidity of these fluids in situ appears to be very sensitive to changes in carbon dioxide tension.
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