The effects of carbogen, carbon dioxide, and oxygen on noise-induced hearing loss

University of Michigan, Ann Arbor, Michigan, United States
Hearing Research (Impact Factor: 2.97). 12/1991; 56(1-2):265-272. DOI: 10.1016/0378-5955(91)90176-A
Source: PubMed


An investigation into the effect of Carbogen (95% O2/5% CO2), 5% CO2/air, and 100% oxygen on cochlear threshold shifts caused by noise was undertaken. Five groups of eight pigmented guinea pigs were exposed to 105 dB broad band noise for 6 h per day for five consecutive days with each group receiving the various gaseous mixtures either during noise exposure or for 1 h immediately after noise exposure. A control group received the same noise exposure but respired air. Auditory threshold shifts, as measured by the auditory evoked brainstem response, were measured at 2,4,8,12,16, 20 and 24 kHz. Recordings were taken pre-exposure and at Day 1, 3, 5, and Weeks 2 and 3 after noise exposure. Carbogen, given during noise exposure, resulted in a trend toward less post noise exposure threshold shift (as compared to controls) which reached statistical significance by Week 3 at all frequencies except 2 and 20 kHz. Subjects given Carbogen after exposure also showed a general trend toward decreased noise induced threshold shifts, as compared to controls, but this was not statistically significant. The mixture of 5% CO2 /air given during noise exposure yielded no difference in threshold shifts as compared to controls. When 100% oxygen was administered during noise exposure, a marked decrease in noise induced threshold shifts could be seen as compared to controls, with differences reaching statistical significance by day 5 at most frequencies. These results indicate that oxygen (i.e. cochlear-oxygenation) is a more important factor than CO2 (i.e., as a vasodilator) in protection of the cochlea from noise induced damage.

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Available from: Alfred Nuttall, May 07, 2015
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    • "This is consistent with the concept that oxygen therapy moderates the effect of an ischaemia from loud sound exposure. Figure 4 shows the considerable reduction of permanent threshold shift that was seen by Hatch et al. (1991). The enrichment of the blood with oxygen would compensate for low flow. "
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    ABSTRACT: This review will briefly examine evidence supporting the hypothesis that sound causes changes in cochlear blood flow, intracochlear oxygen levels, and the morphology of cochlear blood vessels. A survey of the literature shows that traditional histopathological studies provided such evidence and that decreased cochlear blood flow can be demonstrated and measured by laser Doppler flowmetry and by direct observation of cochlear microvessels. Oxygen levels also decline and possibly to a greater degree than blood flow. There is also evidence that in certain circumstances sound can increase blood flow. Reduced blood flow, or reduced oxygenation, is critically important in an organ system with high energy needs like the cochlea. Therefore, a second hypothesis, that sound-induced reduction in CBF represents a functional ischemia, will be explored in examining the relevance of traditional ischemia/reperfusion models to cochlear damage. It is found that reactive oxygen species (free radicals and oxidizing ions) are present in sound-induced hearing loss and thus there is evidence that an ischemia/reperfusion type of injury occurs during loud sound exposures.
    Noise and Health 02/1999; 2(5):17-32. · 1.48 Impact Factor
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    ABSTRACT: The effects of carbogen (5% CO2:95% O2) 10% CO2-in-air and 100% O2 on cochlear blood flow (CBF), skin blood flow (SBP), blood pressure (BP) and arterial blood gases were investigated in the anesthetized, respired or self-respiring guinea pig. In respired animals, CBF and SBF were increased with carbogen and 10% CO2-in-air and decreased with O2. BP was elevated with each gas. In freely breathing animals, only 10% CO2-in-air caused a small increase in CBF; both carbogen and O2 caused CBF to decrease. SPF changes were similar in form, but larger than those seen in respirated subjects. No consistant change in BP was seen during breathing of these mixtures.Arterial PO2 was increased by carbogen and 10% CO2-in-air for both groups. PCO2 increased for both CO2 gas mixtures during forced respiration; but in free-breathing animals PCO2 only increased for 10% CO2-in-air (normal PCO2 values were maintained with carbogen thorough increased breathing rate). The observed changes in CBF were consistant with a balance between a combined vasoconstrictive effect of PO2 and vasodilation effect of PCO2 on cochlear vessels. Analysis of cochlear vascular conductivity (CBF/BP) indicated that vasodilation was significant only with 10% CO2-in-air in respirated animals. In all other conditions the increased CBF apparently reflects the increase profusion pressure associated with respiration of each gas. For clinical purposes, while carbogen does not appear to directly cause vasodilation of cochlear vessels it does lead to an increased oxygenation of the cochlea blood and would appear to avoid the cochlear vasoconstriction caused by 100% O2.
    Hearing Research 11/1991; 55(2-55):255-262. DOI:10.1016/0378-5955(91)90110-U · 2.97 Impact Factor
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