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Yves Cazals

Publications and source records attributed to Yves Cazals.

6 recordsLinked to original sources

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.

Acoustic Stimulation↗

Stress hormones in Ménière's disease and acoustic neuroma.

Stress has been postulated to trigger or contribute to inner ear pathologies but there is little objective evidence. We investigated stress hormones in Ménière's patients and patients with acoustic neuroma. Data were compared with those from a control group of patients with facial spasm. We assayed classic stress hormones including adrenocorticotropic hormone, cortisol, growth hormone and prolactin. We found a strong positive correlation between cortisol and adrenocorticotropic hormone in Ménière patients and patients with acoustic neuroma but no correlation in patients with facial spasm. The data also revealed in female patients with Ménière's disease or with acoustic neuroma an unexpected significant positive correlation between cortisol and prolactin. The data showed the expected negative correlation or no correlation between cortisol and prolactin associated with males and females in the other patient groups. Both cortisol and prolactin increases are known to represent alternative strategies to cope with stress, and our data point to prolactin being possibly more dominant in Ménière's disease and cortisol in acoustic neuroma. These data provide further evidence for modification of different stress hormones in audiovestibular pathologies, which might provide a valuable diagnostic or prognostic tool in the future.

Adrenocorticotropic Hormone↗

Hexachlorobenzene, a dioxin-like compound, disrupts auditory function in rat.

Hexachlorobenzene (HCB) is a dioxin-like compound widely distributed in the environment. In this study, we investigated the effects of HCB on the cochlea. Conscious free-moving rats were given HCB per os daily for 4 weeks at doses of 0.16, 4 or 16 mg/kg in olive oil, whereas the control group received olive oil only. The effects of HCB were evaluated at various time intervals, by measuring auditory nerve acoustic thresholds and plasma thyroid hormone concentration by radioimmunoassay. Histological evaluation involved surface preparation and scanning electron microscopy observations of cochlear hair cells. At a dose of 0.16 mg/kg, HCB induced no loss of acoustic sensitivity, whereas at 4 mg/kg, it induced cochlear sensitivity deficits at the mid-frequencies (2-16 kHz) with complete recovery once treatment was stopped. At a dose of 16 mg/kg, permanent threshold shifts were observed at all frequencies tested (from 1 to 32 kHz). Morphological studies showed no cochlear hair cell loss or alteration of stereocilia. HCB treatment reduced circulating thyroxine concentrations. Thyroidectomy had no effect on cochlear sensitivity in control animals. Thus, HCB is a potent oto-toxicant, and its ototoxicity may be independent of its thyroidal effects.

Animals↗

Does repeated hyperbaric exposure to 4 atmosphere absolute cause hearing impairment? Study in Guinea pigs and clinical incidences.

HYPOTHESIS: Direct pressure applied on the inner ear cannot induce hearing loss. BACKGROUND: Three possible causes have been described in the literature for inner ear permanent lesions during scuba diving: pressure imbalance between the middle ear and the external ear, appearance of microbubbles in the internal ear, and direct effect of pressure on the inner ear. We seek to determine whether this last factor can be involved. METHODS: We submitted two groups of guinea pigs previously implanted with an electrode in the round window to a protocol of air diving in a hyperbaric chamber. Eardrums of animals in one of the two groups had been perforated beforehand. Twenty dives were practiced over 4 weeks. We chose dive parameters consistent with common sport diving: maximal pressure of 4 atmosphere absolute and duration of 30 minutes. Auditory threshold and cochlear spontaneous activity were recorded at regular intervals. Furthermore, we recorded spontaneous cochlear activity in Heliox 400-m and 600-m dives to determine whether our conclusions hold for "extreme" diving. RESULTS: In the group with perforated eardrums, no variation of those parameters were recorded, even in extreme diving. Important variations were noticed in the other group. CONCLUSIONS: Pressure applied directly on the inner ear during diving does not disturb cochlear activity.

Animals↗

Similar half-octave TTS protection of the cochlea by xylazine/ketamine or sympathectomy.

Cochlear efferents, sympathetic control and stress conditions have been shown to influence sound-induced hearing loss. These factors are also known to be modified by sedation/anesthesia. We tested here the effect of sedation/anesthesia on temporary threshold shift (TTS) compared to that in the same awake animals. The effect of sympathectomy was also tested. We employed awake guinea pigs with a chronically implanted electrode on the round window of each of the cochleae. Each ear was tested for its sensitivity to TTS induced by a 1 min or a 10 min exposure to an 8 kHz pure tone at 96 dB sound pressure level. After an intramuscular injection of xylazine or ketamine together with xylazine, TTS at half-octave frequencies was reduced compared to that in awake animals. The second half-octave frequencies were less affected. This specific pattern of protection was also observed here after surgical ablation of a superior cervical ganglion. The data lead to the speculation that protection from TTS under sedation/anesthesia might be due to diminished sympathetic influence. Xylazine is a pre-synaptic alpha2-adrenoreceptor agonist which blocks noradrenaline release from the sympathetic system. Ketamine is a N-methyl-D-aspartic acid receptor antagonist which could reduce glutamate excitotoxicity as well as reduce sympathetic activity.

Adrenergic alpha-Agonists↗

Prolactinoma in some Ménière's patients--is stress involved?

Dizziness is a common complaint in primary care clinics and can enter the diagnostic profile of different pathologies spanning from psychiatric problems to vestibular dysfunction. Episodes of vertigo in Ménière's patients are often reported to be triggered by stress but no physiological data are available to account for the subjective link. The study involved 42 Ménière's patients hospitalized for neurectomy of the vestibular nerve for relief of incapacitating vertigo. In addition 18 patients with neurinoma of the vestibular nerve and 12 patients with facial spasm, who underwent surgery, served as controls. A blood sample was taken on the day of surgery in order to determine the level of battery of different stress hormones. The most striking observation was the presence of hyperprolactinemia (above 20 microg/l) in 14 Ménière's patients. The presence of prolactinoma was confirmed by MRI in six cases out of six investigated and the others have not yet been followed up in this retrospective study. These observations are clearly indicative for systematic determination of prolactin levels before opting for surgery in Ménière's patients.

Adult↗