Intensity-related changes in cochlear blood flow in the guinea pig during and following acoustic exposure

Abstract

This study examined the effects of acoustic exposure at different intensities on cochlear blood flow (CBF) using laser Doppler flowmetry. CBF was measured in anesthetized guinea pigs exposed to either a 10 kHz pure tone at 125, 105, or 90 dB SPL, or wide-band noise at 85 dB SPL for 1 h. Mean arterial blood pressure and heart rate were recorded continuously. Arterial acid-base status, cochlear temperature, cochlear microphonics (CM), and compound action potentials (CAP) were measured before and after exposure. There was a small, but significant, steady decline in basal CBF after 40 min loud sound exposure (125 dB SPL), but no change in basal CBF occurred with the lower intensities (85-105 dB SPL). In contrast, there was a significant increase in apical CBF after 1 h exposure to either moderate wideband noise (85 dB SPL) or a 10 kHz tone at 105 dB SPL. These changes persisted during a 20-min post-exposure period. In most cases, the cochlear temperature and cardiorespiratory variables monitored remained unchanged during and after the exposures as compared to the controls. CM and CAP amplitudes showed extensive losses after acoustic overstimulation (125 dB SPL), but no permanent changes were found at the lower intensities used. The present findings confirm the occurrence of intensity-related effects of acoustic exposure on the cochlear microcirculation.

8-Iso-Prostaglandin F_2α, a Product of Noise Exposure, Reduces Inner Ear Blood Flow

“…9), noise exposure produced significant reductions (p ! 0.05) in basal turn CBF as measured by VC, in agreement with previous reports of the effects of noise on CBF [Scheibe et al, 1993;. The maximum mean vasoconstriction was 27B7% below baseline.…”

“…At very high sound exposure levels (120-155 dB), the reduction in cochlear blood flow (CBF) and local vasoconstriction can be quite dramatic [Perlman and Kimura, 1962;Quirk et al, 1992], such that the cochlea is subject to severe hypoperfusion. The observed vascular changes affect the major arterioles supplying the cochlea, as well as the radiating arterioles and capillary beds [Hawkins, 1971;Axelsson et al, , 1983, resulting in decreased CBF Scheibe et al, 1993], vasoconstriction [Hawkins, 1971;Vertes et al, 1981;Quirk et al, 1992], aggregation of red blood cells [Hawkins, 1971;, and increased pericyte diameter .…”

Mechanisms of noise-induced hearing loss indicate multiple methods of prevention

“…Until a decade ago, the prevailing view of NIHL was that it was caused by mechanical destruction of the delicate membranes of the hair cells and supporting structures of the organ of Corti (Spoendlin, 1971;Elliott, 1972,1973;Hunter-Duvar and Bredberg, 1974;Hawkins et al, 1976;Mulroy et al, 1998), with perhaps some effect of intense noise on blood flow to the inner ear (Perlman and Kimura, 1962;Hawkins, 1971;Hawkins et al, 1972;Lipscomb and Roettger, 1973;Santi and Duvall, 1978;Axelsson and Vertes, 1981;Axelsson and Dengerink, 1987;Duvall and Robinson, 1987;Scheibe et al, 1993;Miller et al, 1996). We now know another significant factor is intense metabolic activity, which increases mitochondrial free radical formation.…”

Free radical scavengers vitamins A, C, and E plus magnesium reduce noise trauma

“…Identification of this safe and effective antioxidant intervention that attenuates NIHL provides a compelling rationale for human trials in which free radical scavengers are used to eliminate this single major cause of acquired hearing loss. Keywords cochlea; free radical; noise; hearing; antioxidant; vasodilation Mechanical destruction of cells in the organ of Corti was once assumed to be the primary cause of noise-induced hearing loss (NIHL) [1][2][3][4][5][6][7][8], with perhaps some effect of reduced blood flow to the inner ear [9][10][11][12][13][14][15][16][17][18]. We now know that another key factor is intense metabolic activity that results in production of excess free radicals [19][20][21][22][23] and lipid peroxidation products [24].…”