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PubMed1991

Strial circulation impairment due to acoustic trauma.

Blood circulation in the cochlear lateral wall after exposure to a non-physiological level of sound (120-125 dB SPL, 3 h) was investigated immunohistologically. Kanamycin (KM), which was expected to function as a tracer of blood flow, was administered to guinea pigs 5 min to 21 h after sound termination. At 5-30 min, KM was scarce in the capillaries of the stria vascularis (CSVs), whereas abundant KM was present in the spiral ligament vessels. These findings differed markedly from those in non-sound-exposed animals. After the initial period, KM gradually did enter into the CSVs, but its pattern of existence there differed from the normal pattern. These observations suggest that acoustic trauma causes blood stagnation in the strial capillaries, leading to strial dysfunction.

Animals↗
PubMed1986

[A method for relieving tinnitus complaints in long-enlisted soldiers with multiple acoustic traumas--external electrostimulation].

The effect of external electrostimulation (EES) on tinnitus in soldiers with multiple blast trauma was assessed in a controlled study. There was no change in the tinnitus in the untreated control group during an observing period of 5 weeks. However the noise resolved completely within 28 days of therapy in 20% of treated soldiers, in some patients the symptoms were improved. The repeated application of EES is effective in recurrent complaints. This method can be carried out on an out-patient basis and scarcely has any side-effects. It is not suitable for treating tinnitus after acute acoustic trauma.

Adult↗
PubMed2006

Glucocorticoid receptors modulate auditory sensitivity to acoustic trauma.

Glucocorticoids are widely used to treat different hearing disorders yet the exact mechanisms of glucocorticoid action on the inner ear are not known. The inner ear of both humans and experimental animals demonstrate an abundance of glucocorticoid receptors (GRs) in both neuronal and non-neuronal tissues. In this review, we discuss how activation of the hypothalamic-pituitary-adrenal axis can directly modulate hearing sensitivity. Recent findings indicate that several factors define the responsiveness of the peripheral auditory system to glucocorticoids including the concentration of agonist, availability of the GR, and the activation of GR and NF-kappaB. These findings will further our understanding of individual glucocorticoid responsiveness to steroid treatment, and will help improve the development of pharmaceuticals to selectively target GR in the inner ear for individuals with increased sensitivity to acoustic trauma.

Animals↗
PubMed1983

Lifelong susceptibility to acoustic trauma: changing patterns of cochlear damage over the life span of the mouse.

Age-related differences in susceptibility to noise-induced threshold shift (NITS) were examined over the entire life span of the CBA/J mouse. Mice of varying ages were given a single 5-min exposure to a 124-dB octave-band (12-24 kHz) noise. Susceptibility began at 15-16 days postpartum and increased rapidly until approximately 20 days of age. During this phase, NITS (as measured by increased action potential threshold) was greatest at 16 kHz. Overall susceptibility was consistently high from 20 to 90 days. During this phase, NITS became most severe at 32 kHz. From 120 days until beyond the end of its actuarial life span (527 days), NITS no longer occurred at 2-16 kHz, but the 64-kHz response retained its susceptibility to acoustic trauma. Mice at 20 and 60 days of age showed the same pattern of decreasing susceptibility as the intensity of the noise exposure was reduced to 114 and 104 dB, indicating that the absence of a tightly restricted critical period is not peculiar to a particular sound pressure level.

Age Factors↗
PubMedDate not supplied

[New therapeutic prospects in acute acoustic trauma].

A total of 50 young soldiers hospitalized for high frequency hearing loss and tinnitus following exposure to gun impulse noise was studied in order to ascertain the effects of two kinds of medical treatment. A first group (18 subjects) was treated for 10 consecutive days with cerebral gangliosides. In a second group (17 subjects) gangliosides were associated with subcutaneous infiltration of bupivacaine chlorhydrate (0.5%). A third group (15 subjects) was taken as control. An improvement in hearing threshold (= greater than 20 dB at 4-8 kHz) and a consistent relief of tinnitus was respectively found in 52% and 66% of the treated subjects, while hearing status and tinnitus persisted unchanged among the control group subjects. The amount of hearing improvement over the control group proved to be statistically significant, although no significant difference was demonstrated between the two kinds of medical treatment. Since therapy was initiated 5 to 21 days after acoustic trauma, these results indicate that a pharmacological treatment may be effective even in cases where diagnosis is forwarded relatively late in respect to the trauma.

Adult↗
PubMedDate not supplied

Effect of acoustic trauma on cytochrome oxidase activity in stria vascularis.

The present study was undertaken to determine the role of metabolic disturbance in noise-induced hearing loss by histochemical studies of cytochrome oxidase activity. Adult normal albino guinea pigs were used. The experimental animals were exposed to broad-band noise at 105 dB SPL for 24 h. The control animals were not exposed to the noise. The thresholds of the auditory brainstem response (ABR) of all guinea pigs were measured 3 times: before noise exposure, 1 day and 1 month later. The difference between the ABR thresholds before and after noise exposure was statistically significant. Vibratome sections of decalcified cochleae of the noise-exposed (n = 8) and control groups (n = 4) were incubated with Spector's medium and embedded with Epon. Thin sections (2 microm) and ultrathin sections (100 nm) were cut to observe cytochrome oxidase activity in the stria vascularis under light and electron microscopes, respectively. A decreased activity of cytochrome oxidase was consistently shown in the normal-appearing stria vascularis of most noise-exposed ears. Acoustic trauma has an adverse effect on cytochrome oxidase activity in the stria vascularis as well as on hearing. A decrease in the activity of cytochrome oxidase implicates that metabolic damage may play a role in noise-induced hearing loss.

Animals↗
PubMed2002

Effects of acoustic trauma on dorsal cochlear nucleus neuron activity in slices.

Previous studies found increased multi-unit spontaneous activity in the dorsal cochlear nucleus (DCN) of animals that had been exposed to intense sound. Such activity may be related to tinnitus. Our study examined effects of previous exposure to intense sound on single neurons in the DCN, by measuring spontaneous activities and sensitivities to acetylcholine, an important neurotransmitter of centrifugal pathways to the cochlear nucleus, in brain slices. Spontaneous discharges were recorded extracellularly in the DCN portion of brain slices from control and intense-tone-exposed rats. Slices from exposed rats showed increased prevalence of bursting and decreased regular spontaneous activity. Since regular neurons include fusiform cells, and bursting neurons include cartwheel cells, intense tone exposure may lead to increased activity of DCN cartwheel cells and decreased activity of fusiform cells. Alternatively, the activity of some fusiform cells might change to bursting. Intense tone exposure also appeared to increase bursting neuron sensitivity to carbachol. This suggests that changes in DCN cartwheel cell spontaneous activity may reflect changes in effects of cholinergic centrifugal pathways following intense tone exposure. We conclude that acoustic trauma may lead to changes in the physiology and pharmacology of DCN neurons. These changes may be related to underlying mechanisms of central tinnitus.

Animals↗
PubMed2003

[Changes in antioxidant capacity of the guinea pig exposed to noise and the protective effect of alpha-lipoic acid against acoustic trauma].

The study was aimed at exploring the effect of noise on total antioxidant capacity (TAC) in serum, nitric oxide (NO) level in the cochlea and the protective action of alpha-lipoic acid against noise-induced hearing loss (NIHL). Sixty guinea pigs (350-400 g) were divided randomly into three groups (control group, noise+saline group and noise+alpha-lipoic acid group). Serum and cochlear tissue were treated immediately after noise exposure (4-kHz octave band, 115 dB SPL 5 h) to determine the level of TAC and NO, respectively. Auditory brainstem responses (ABRs) were measured before and immediately after exposure. The threshold of hearing in the control group was relatively stable, while the hearing threshold in the noise+saline group was significantly higher than those in the noise+alpha-lipoic acid group (P<0.05). TAC level of the noise+saline group was significantly lower than that of the control group P<0.05 . TAC level of the noise+alpha-lipoic acid group was significantly higher than that of the noise+saline group P<0.05 , while there was no significant difference in the levels between the noise+alpha-lipoic acid group and the control group (P>0.05). The NO level of the cochlear tissue in the noise+saline group was significantly higher than that of the control group (P<0.05). Cochlear NO level in the noise+alpha-lipoic acid group was significantly lower than that of the noise+saline group (P<0.05), while there was no significant difference in cochlear NO levels between the noise+alpha-lipoic acid group and the control group (P>0.05). The results obtained indicate that noise exposure causes a decrease in serum TAC and an increase in NO in cochlea. alpha-Lipoid acid exerts a protective effect against hearing loss in acoustic trauma through its antioxidant effects.

Animals↗
PubMed1997

New growth of axons in the cochlear nucleus of adult chinchillas after acoustic trauma.

This study determined the effect of acoustic overstimulation of the adult cochlea on axons in the cochlear nucleus. Chinchillas were exposed to an octave-band noise centered at 4 kHz at 108 dB sound pressure level for 1.75 h. One chinchilla was never exposed to the noise, and several others had one ear protected by an ear plug or prior removal of the malleus and incus. Exposure of unprotected ears caused loss of inner and outer hair cells and myelinated nerve fibers, mostly in the basal half of the cochlea. Cochlear nerve fiber degeneration, ipsilateral to the exposed ears, was traced to regions of the cochlear nucleus representing the damaged parts of the cochlea. In silver impregnations of a deafferented zone in the posteroventral cochlear nucleus, the concentration of axons decreased by 43% after 1 month and by 54% after 2 months. However, by 8 months, the concentration of thinner axons, with diameters of less than 0.46 microm, increased by 46-90% over that at 2 months. The concentration of axons with larger diameters did not change. Between 2 and 8 months small axonal endings appeared next to neuronal cell bodies. This later increase of thinner axons and endings is consistent with a reactive growth of new axons of relatively small diameter. The emergence of small perisomatic boutons suggests that the new axons formed synaptic endings, which might contribute to an abnormal reorganization of the central auditory system and to the pathological changes that accompany acoustic overstimulation.

Animals↗
PubMed1964

ACOUSTIC TRAUMA.

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Canada↗
PubMed1963

ACOUSTIC TRAUMA.

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Blood Circulation↗