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Biomedical subjects

J Kusakari

Publications and source records attributed to J Kusakari.

141 records · Page 8Linked to original sources
PubMedDate not supplied

Ionic changes in cochlear endolymph of the guinea pig induced by acoustic injury.

The effects of acoustic overstimulation on the endocochlear potential (EP) and on concentrations of ions (K+, Na+, Cl-, H+, HCO3-, and Ca2+) in endolymph were investigated using ion-selective microelectrodes. A slight but significant elevation of the EP and alkalinization of the endolymph were induced by acoustic overstimulation, whereas there was little change in the K+, Na+, Cl-, and HCO3- concentrations. The changes in H+ and HCO3- concentrations implied a depression of PCO2, suggesting an increase in blood flow to the cochlea. On the other hand, the Ca2+ concentration increased abruptly to 48 times the pre-exposure value. In contrast, no significant change in the Ca2+ concentration was observed in cochleae with damaged hair cells. We discuss the mechanism of the tone-induced Ca2+ elevation in endolymph and its effect on hearing acuity.

Animals↗
PubMedDate not supplied

N1 latency prolongation in the guinea pig cochlea treated with nitrogen mustard-N-oxide studied by narrow band analysis.

The effect of nitrogen mustard-N-oxide (NMO) upon the click and tone burst-evoked N1 latency was examined in 14 albino guinea pigs. In all animals except one, the pseudothresholds of action potentials were elevated, especially in the high tone area. In addition to the amplitude reduction, the N1 latency was prolonged in 12 animals. The narrow band analysis of N1 revealed that the latency was equally prolonged in all frequency areas, although the amount of the amplitude reduction was much larger in the high frequency area. It was concluded that the prolongation of the N1 latency in NMO-treated animals was due to dysfunction of outer hair cells along the entire cochlear partition.

Acoustic Stimulation↗
PubMedDate not supplied

Reduction of the endocochlear potential by the new "loop" diuretic, bumetanide.

The effect of bumetanide upon the endocochlear potential (EP) was examined in 46 guinea pigs. The EP was reduced with dosages of 5 mg/kg or more. The maximum depression of the EP (reduction to -30 to -40 mV) was obtained at a dosage of 30 mg/kg. The recovery of the potential was incomplete at any dosage within three hours and the response pattern of the EP to bumetanide was similar to that to ethacrynic acid. The present experiments revealed that bumetanide, by weight, has a stronger ototoxic potency than the other "loop" diuretics--furosemide and ethacrynic acid. However, the diuretic effect of 1 mg bumetanide is equivalent to 40 to 60 mg furosemide or ethacrynic acid. Therefore, the relative ototoxic potency of bumetanide is much smaller suggesting that from a clinical standpoint bumetanide is much safer than the other "loop" diuretics.

Action Potentials↗
PubMedDate not supplied

Saccular and cochlear endolymphatic potentials in experimentally induced endolymphatic hydrops of guinea pigs.

Saccular and cochlear endolymphatic potentials (SEP and CEP) were recorded in 33 normal animals. We confirmed that SEP is not produced in the saccule per se, but is a potential leak from the cochlea. CEP was reduced to one-tenth of the original value when it reached the saccule. Endolymphatic hydrops was provoked in 32 animals, and CEP and SEP were successfully recorded in 29 and 20 cases, respectively. The measurements were performed in the 2nd, 4th and 12th postoperative week. Both CEP and SEP decreased in magnitude as time elapsed after the surgery. This reduction is attributed to the strial dysfunction. In advanced hydrops, CEP transmission to the saccule is greatly inhibited. It is concluded that the saccular dysfunction can occur in the hydropic ear.

Animals↗
PubMedDate not supplied

The effect of the cationic composition in perilymph upon the N1 latency of the guinea pig.

Although a suitable cationic composition in perilymph is known to be essential for the generation of N1, the effect of the cationic change upon the N1 latency has never been investigated in detail. The scala tympani was perfused with an artificial perilymph with a high K+, low Na+ or low Ca2+ content, with simultaneous measurement by an ion-selective microelectrode to observe its effect upon the N1 latency. An excess of K+, a depletion of Na+ and a depletion of Ca2+ in perilymph individually suppressed the N1 amplitude and elevated the N1 threshold. The N1 latency was not prolonged in the high K+ group but the significant prolongation was observed in the other two groups.

Animals↗