Reduction of acoustically induced auditory impairment by inhalation of carbogen gas. II. Temporary pure-tone induced depression of cochlear action potentials.
Guinea pigs were exposed to a 4.5 kHz pure-tone at 104 dB for 10 min during artificial ventilation with either carbogen gas (95% O2/5% CO2) or normal air. Mean N1 response amplitudes to tone bursts at 32 test frequencies extending from 2.1 kHz through 30 kHz were measured at standardized intervals before and after the acoustic overstimulation. All animals received normal air during recovery. Significant reduction of N1 response amplitude depression within a 3/8 to 1 octave frequency domain above the exposure frequency was found in the group which received the carbogen gas. Those frequencies found to be maximally depressed and the relative rate of recovery from the acoustic overstimulation were not affected by carbogen inhalation. The invariance of the "half-octave shift" following pure-tone acoustic overload was confirmed. Arterial blood gas analysis of guinea pigs respiring carbogen revealed a marked rise in PO2 and PCO2. Carbon dioxide is a potent stimulator of cerebral and cochlear vasodilatation. Sound-induced vasoconstrictive ischemia has been implicated in noise-induced cochlear pathology. The beneficial effects of elevated arterial PCO2 are suggested to have been mediated by reduction of acoustically induced vascular insufficiency within the inner ear.
D000818:Animals; D002245:Carbon Dioxide / Q000627:therapeutic use*; D003051:Cochlea / Q000098:blood supply; D003055:Cochlear Microphonic Potentials; D005072:Evoked Potentials, Auditory; D006168:Guinea Pigs; D006317:Hearing Loss, Noise-Induced / Q000503:physiopathology / Q000628:therapy*; D010100:Oxygen / Q000627:therapeutic use*; D012138:Respiratory Therapy; D013268:Stimulation, Chemical; D013997:Time Factors; D014664:Vasodilation / Q000187:drug effects; D000159:Vestibulocochlear Nerve / Q000503:physiopathology
D002245:Carbon Dioxide; C011700:carbogen; D010100:Oxygen