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In 14 guinea pigs the pO2 in the perilymph of the scala tympani fell to 50%-80% of the original value during exposure to noise consisting of 4,000 Hz clicks with a repetition rate of 20/s, 100 dB CHL = 120 dB SPL p.e., repeated twice over a period of 24 minutes each time. For the measurements of the pO2 we used the thin 0.5 micron micro-coaxial needle electrode described by Baumgärtl and Luebbers, which was placed through the round-window membrane in the scala tympani to a depth of 600 micron. The simultaneously recorded CAP latency times were prolonged by 0.8 ms at a test loudness of 60 and 80 dB CHL. The amplitudes of the CM had declined by 60%-70% of the original values at a test loudness of 80 dB SPL p.e. The intra-arterial blood pressure in the common carotid artery of all animals remained constant. As the cortilymph spaces communicate with the perilymph of the scala tympani, our measured decline of pO2 in the perilymph could indicate a cortilymph hypoxia. During exposure to noise the oxygen-dependent Na+ and K+ pumps, which maintain the ion balance and function of the organ of Corti, can decompensate due to lack of oxygen. That would lead to a K+ contamination of the cortilymph and to an intracellular Na+ accumulation, which can cause microstructural damage (hair cell-cilia fusion, hair cell, synaptic and dendritic swelling, hair cell contraction and sustained depolarization), which would be reflected in the CMs and CAPs.

Our earlier animal experiments on guinea pigs showed that instrumental perforation of the round window membrane by a 0.2 mm platinum wire leads to an instant loss of the inner ear functions. The membrane defect healed in a few days, the cochlear structures remained intact, and the compound action potential of the auditory nerve and the brain-stem responses could be evoked again with normal latency times within 2 weeks. 1. In the studies reported here we first carried out microperforations with a 1 micron needle electrode, which caused no changes of the hearing potentials (cochlear microphonics, compound action potential of the auditory nerve, brain-stem responses), and no visible defect of the round window membrane and no perilymph outflow. 2. The removal of the round window membrane and the withdrawal of the perilymph led to a loss of the cochlear microphonics and to a considerable increase of the latency times of wave I (Jewett). The hearing potential regained their original values after 2 weeks without closure of the round window niche. The round window membrane had regenerated spontaneously and the scala tympani was again filled with perilymph. After covering the round window niche with a connective tissue graft, the hearing potentials regained their original values after 2 weeks, as they had done without cover of the round window niche. The round window membrane regenerated below the tissue graft and the scala tympani was also filled again with perilymph.(ABSTRACT TRUNCATED AT 250 WORDS)

The purpose of this study was to examine the influence of hyperbaric oxygen on the oxygen tension (pO2) in the normal inner ear. We examined 16 anaesthetised guinea pigs by means of an oxygen-sensitive micro-coaxial needle electrode, using the method described by Baumgaertl and Luebbers. In all animals the pO2 in the perilymph of the scala tympani fell by 34% of the original value during insertion of the sensor into the scala tympani. After we had flooded the hyperbaric chamber with pure oxygen under normobaric conditions the pO2 increased by 244.3% of the original values. Furthermore the pO2 increased by 9.4 times the original values during hyperbaric oxygen at 1.6 bar.

Nineteen guinea pigs were exposed to impulse noise from gunfire (G3 of the Federal German Army, 156 dB peak SPL), 6+6 shots or 12+6 shots, with a 3-s pulse interval. For simultaneous measurements of pO2, cochlea microphonics (CM) and compound action potentials of the auditory nerve (CAP), we used the thin 0.5 microns microcoaxial needle electrode described by Baumgaertl and Luebbers, which was placed through the roundwindow membrane into the scala tympani to a depth of 1000 microns. After exposure to the first 6 or 12 gunshots, the pO2 increased by about 20% of the original values in 12 guinea pigs (63%). In the following 30 min of recovery time the pO2 decreased, stabilized or showed a further decline. There were only 3 animals with a pO2 loss of 70% of the original values. Most animals showed a decline of 25% at the end of the recovery period. In all animals after 6 additional shots, the pO2 only decreased by another 5% of the original values. Amplitudes of CM and CAP were reduced by about 40% of the original values after 6 or 12 shots and by another 20%-24% (CM) and 5%-15% (CAP) after 6 additional shots. The intra-arterial blood pressure in the common carotid artery remained constant. The results are discussed with respect to the well-known morphological damage, subsequent ion imbalance and hypoxia within the cortilymph after exposure to gunfire. These changes are reflected in the loss of CMs and CAPs.