Loudness reduction induced by a contralateral tone.

The induced reduction in the loudness (ILR) of a weaker tone caused by a preceding stronger tone was measured with both tones in the same ear (ipsilateral ILR) and also in opposite ears (contralateral ILR). The two tones were always equal in duration and were presented repeatedly over several minutes. When the tone duration was 200 ms, for 24 listeners the loudness reduction averaged 11 dB under ipsilateral ILR and 6 dB under contralateral ILR. When the duration was 5 ms, ILR was 8 dB whether ipsilateral or contralateral. For each duration, ipsilateral and contralateral ILR were strongly correlated (r around 0.80).

Hyperbaric oxygenation with corticoid in experimental acoustic trauma.

Among possible therapies after acute acoustic trauma, hyperbaric oxygenation (HBO) combined with corticoid was found effective in several animal studies. Such evidence was obtained for moderate 20-25 dB losses. The aim of this study was to further assess this therapy for noise-induced hearing losses greater than previously examined. Sixty-five ears from thirty-six adult guinea pigs were used. Acoustically evoked responses from intracranial electrodes chronically implanted bilaterally into the ventral cochlear nucleus were used to assess acoustic sensitivity alterations. Trauma sound was a third-octave noise-band around 8 kHz presented bilaterally at 115 dB SPL for 45 min. One control group received no treatment, one group was treated with HBO only and another with corticoid only both starting within one day post-trauma, two groups were treated with both HBO and corticoid starting for one group within one day post-trauma, and for the second group at 6 days post-trauma. Acoustic thresholds were measured between the 6th and the 16th days after acoustic trauma. Animals treated with HBO alone or corticoid alone did not differ from controls. Combined HBO and corticoid therapy provided significant protection from noise-induced loss of auditory thresholds, especially when started one day post-exposure. Hearing loss reduction induced by HBO combined with corticoid was of similar magnitude (about 10-15 dB) as in previous studies although the induced hearing loss was considerably greater (about 40 dB instead of 20-25 dB).

Enhanced cochlear acoustic sensitivity and susceptibility to endotoxin are induced by adrenalectomy and reversed by corticosterone supplementation in rat.

Glucocorticoid receptors are widely distributed in the cochlea but their role remains poorly known. Previous studies provided contradictory reports on a possible cochlear acoustic hypersensitivity induced by adrenal insufficiency, while several experiments agree on a significant action of glucocorticoid receptors in adverse conditions such as acoustic trauma and restraint stress. The present experiments confirmed a cochlear acoustic hypersensitivity induced by adrenalectomy and reversed by corticosterone supplementation. These observations point to a significant role of corticosteroids in basal cochlear functioning. The glucocorticoids are known to be essential for limiting and resolving inflammatory processes. The endotoxin Escherichia coli lipopolysaccharide is widely used to induce inflammatory reactions. However, in various organs several toxic processes of this endotoxin are not influenced by glucocorticoids. From previous experiments on the cochlea there is no evidence that glucocorticoids are an essential factor against endotoxin cochlear toxicity. In the present experiments it was found that adrenalectomy greatly increased the cochlear susceptibility to endotoxin; the effect was reversed by providing corticosterone supplementation. This shows the essential role of corticosterone in this cochlear inflammation model. In previous studies local administration (at the cochlear base) of endotoxin was used and losses of cochlear acoustic sensitivity were found predominantly at high frequencies; in contrast, the systemic injection used in this study produced a cochlear loss of acoustic sensitivity at all frequencies, indicating a uniform cochlear sensitivity to the toxic effects of endotoxin.