Takayuki Nakano

Effects of Kanamycin Sulfate on Cochlear Potentials and Potassium Ion Permeability through the Cochlear Partitions

The cochlear microphonics (CM), endocochlear potential (EP) and potassium ion activities in the endolymph and perilymph were measured in guinea pigs which received daily successive intramuscular injections of 500 mg/kg of body weight of kanamycin sulfate. Preyers reflex threshold at 8 kHz began to increase after the 5th day of kanamycin treatment and disappeared on the 11th day. The maximum output of CM at 8 kHz began to decrease with a time course similar to Preyers reflex. The potassium ion activities in the endolymph and perilymph and the EP did not change appreciably through all experimental days. The magnitude of the negative EP decreased in parallel with the reduction in CM and the relative potassium conductance (GK) between the endolymph and perilymph. These results lend support to the hypothesis that the site of production of the negative EP is probably in the hair cells and that the negative EP is mainly dependent on the permeability of the potassium ions in the organ of Corti.

Effects of Various Vanadium Compounds on Cochlear Potentials

The effects of vanadium compounds, sodium vanadate, ammonium vanadate, potassium vanadate, vanadium oxysulfate, vanadium acetylacetonate, and vanadium trichloride, on endocochlear potential (EP) and cochlear microphonic potential (CM) were examined in the guinea pig cochlea. The perilymphatic space was perfused for 30 min with 1 mM solution of each compound and changes of EP, CM, and negative EP were observed. Upon perfusion with pentavalent vanadium solutions, such as sodium vanadate, ammonium vanadate, and potassium vanadate, the EP showed an overshoot at the beginning of perfusion and then a gradual decrease, while the CM showed only a gradual decrease. The other compounds had no effects on EP and CM. Since the negative EP showed no differences due to perfusion of any compound, it is concluded that the vanadate compounds have inhibitory effects on EP primarily, and on CM only secondarily. The chemical mechanism of the effects of vanadates was discussed concerning the function of the stria vascularis and also its participation in acute hearing loss.

Antagonistic action of reductants against vanadate-induced EP decrease.

The antagonistic action of ascorbic acid or glutathione against vanadate was studied by observing changes in EP in guinea pig cochlea. After intravenous injection of ascorbic acid or glutathione, the EP decrease induced by perfusion of the perilymphatic space with vanadate solution was suppressed and the EP showed a remarkable recovery in some animals. Intravenous preadministration of either of the two compounds inhibited or prevented the vanadate-induced EP decrease. When ascorbic acid or glutathione was added to the vanadate solution, the EP decrease was also inhibited. The chemical action of both reductants against vanadate is discussed. From the results obtained, it is speculated that a chemical balance between some oxidants and reductants in the stria vascularis, must be kept constant in order to maintain the EP at a constant potential level.

Effects of vanadate on EP and its distribution in guinea pig cochlea.

Effects of sigma-sodium vanadate on endocochlear d.c. potential (EP) and cochlear microphonic potential (CM) were examined and its distribution was observed by an X-ray microanalyzer in the guinea pig cochlea. The perilymphatic space was perfused with 1, 5, and 10 mM solutions of sodium vanadate, using a Harvard Microperfusion pump. By perfusing the scala vestibuli, EP and CM showed a rapid decrease. On the other hand, by perfusing the scala tympani, EP showed an overshoot at first, then a gradual decrease, while CM showed only a gradual decrease. The rates of decrease of EP and CM were dependent upon perfusion time and vanadate concentration. After the electrophysiological examinations, the specimen of the cochlea was observed by X-ray microanalyzer. An accumulation of vanadium was confirmed, especially in the stria vascularis and the hair cells. From the results obtained, the possibility of the responsibility of vanadate for a hypothetical sudden deafness originating in the stria vascularis was discussed.