Noxious effects upon cochlear metabolism

Thalmann, Ruediger; Thalmann, Isolde; Ise, Ikuo; Paloheimo, S.

doi:10.1002/lary.5540870506

Cited by 23 publications

(3 citation statements)

References 45 publications

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“…Patterson & Gulick, 1963), it is unlikely that suppression of cochlear respiratory enzyme activity is the primary mechanism whereby ethacrynic acid (and by implication, furosemide) exerts ototoxic effects. Similar conclusions were drawn, by Thalmann, Thalmann, Ise & Paloheimo (1977) and Kusakari, Ise, Comegys, Thalmann & Thalmann (1978), from data with furosemide.…”

Section: Discussionsupporting

confidence: 72%

The effects of intracochlear and systemic furosemide on the properties of single cochlear nerve fibres in the cat

Evans

Klinke

1982

The Journal of Physiology

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SUMMARY1. Tuning properties and spontaneous discharge rate of single cochlear fibres in the anaesthetized cat were determined during short-and long-term poisoning of the cochlea by locally and systemically applied furosemide.2. With intra-arterial administration offurosemide, short-term reversible elevation occurred of the low threshold sharply tuned 'tip' segment of the frequency threshold ('tuning') curve (f.t.c.) by up to 40 db, without substantial changes in the threshold of the low frequency 'tail' segment of the f.t.c. These changes could occur in part without changes in the spontaneous activity and entirely without changes in the maximal evoked activity. These effects were observed in all fibres examined, the characteristic frequencies of which ranged from 3-5 to 31 kHz.3. Intracochlear administration of furosemide in 0-9 mm concentrations produced similar changes, but these were not reversible.4. The changes correlated with the depression of the amplitude of the gross cochlear action potential. The cochlear microphonic potential, however, was either unchanged, or only slightly reduced.5. In long-term furosemide poisoning of the cochlea, fibres with anomalous response properties were found alongside fibres having normal tuning. The former exhibited either reduced excitability of the low threshold tip segment, or a tip segment attenuated in both excitability and threshold.6. It is concluded that the selective effects of furosemide on the tip segment of cochlear fibre f.t.c.s offer further evidence for a physiologically vulnerable 'second filter' in the cochlea. The selective influence of the furosemide on the low threshold tip segment provides support for the hypothesis that the normal f.t.c. is generated by two largely independent processes: one vulnerable, low threshold and sharply tuned, and the other less vulnerable, but high threshold and more broadly tuned.7. The findings, obtained with an agent known to produce reversible impairment of hearing in man, provide direct physiological evidence in support of the hypothesis that in sensorineural hearing loss of cochlear origin the frequency selectivity of cochlear nerve fibres is impaired.

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Section: Discussionsupporting

confidence: 72%

The effects of intracochlear and systemic furosemide on the properties of single cochlear nerve fibres in the cat

Evans

Klinke

1982

The Journal of Physiology

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“…Previously, the effects of acute energy failure on the cochlea have been studied using anoxia or chemical asphyxiants such as carbon monoxide, cyanide and nitric oxide [Brown et al, 1983;Kong et al, 1996;Nuttall and Lawrence, 1979;Pai et al, 1998;Rao and Fechter, 2000;Ruan et al, 1997;Tawackoli et al, 2001;Thalmann et al, 1977]. In these studies, electrophysiological methods were primarily used to investigate the pathophysiology of cochlear dysfunction, and only a small number of morphological studies limited to the organ of Corti and spiral ganglion cells have been conducted [Kong et al, 1996;Pai et al, 1998;Ruan et al, 1997].…”

Section: Discussionmentioning

confidence: 99%

Permanent Threshold Shift Caused by Acute Cochlear Mitochondrial Dysfunction Is Primarily Mediated by Degeneration of the Lateral Wall of the Cochlea

et al. 2005

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Mitochondrial dysfunction in the cochlea is thought to be an important cause of sensorineural hearing loss. Recently, we have established a novel rat model with acute hearing impairment caused by exposure to the mitochondrial toxin 3-nitropropionic acid (3-NP) to analyze the mechanism of cochlear mitochondrial dysfunction. Both permanent and temporary threshold shifts were observed in this model depending on the amount of 3-NP used to induce hearing impairment. In this study, we demonstrate cochlear morphological changes in the permanent threshold shift model. Marked degeneration was detected in type 2 fibrocytes in the spiral prominence, type 4 fibrocytes in the spiral ligament, marginal cells and intermediate cells in the stria vascularis 3 h after 3-NP administration; these changes were progressive for at least 14 days. Less prominent degeneration was detected in type 1 and type 3 fibrocytes in the spiral ligament. These results indicate that permanent threshold shift caused by acute cochlear mitochondrial dysfunction is primarily mediated by cellular degeneration in the lateral wall of the cochlea, and suggest that therapy of cochlear hearing loss due to acute energy failure may be achieved through protection and regeneration of the cochlear lateral wall.

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“…Rather, it is likely to be due to an increase in an intracellular constituent to which phosphate is bound. Thalmann et al (1977) showed that phosphocreatinine levels rise when Na + -K + ATPase is inhibited by ouabain, and it is possible that a similar increase takes place in hair cells following Cisplatin.…”

Section: Discussionmentioning

confidence: 99%

Early morphological and chemical changes induced by cisplatin in the guinea pig organ of Corti

et al. 1986

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Guinea pigs were treated with a single dose of Cisplatin (5 mg IP). After 2-4 days the cochleas were prepared for morphological analysis by scanning electron microscopy and chemical analysis by X-ray dispersive microanalysis. Following Cisplatin, the bundles of stereocilia on the hair cells were found to be rough, disarrayed, fused, and finally absorbed. Significant increases were found in the levels of calcium, sulphur, and phosphorus in the abnormal hair cells. It is suggested that the high calcium levels might be due to the inhibition of enzymes which normally keep cytoplasmic calcium low, and that some of the changes in the stereocilia might be secondary to this.

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Noxious effects upon cochlear metabolism

Cited by 23 publications

References 45 publications

The effects of intracochlear and systemic furosemide on the properties of single cochlear nerve fibres in the cat

The effects of intracochlear and systemic furosemide on the properties of single cochlear nerve fibres in the cat

Permanent Threshold Shift Caused by Acute Cochlear Mitochondrial Dysfunction Is Primarily Mediated by Degeneration of the Lateral Wall of the Cochlea

Early morphological and chemical changes induced by cisplatin in the guinea pig organ of Corti

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