We examined the effects of anoxia and ethacrynic acid on the endolymphatic potential and cation activity in the superior ampulla of the guinea pig, using double-barrelled ion-exchanger microelectrodes. In normal guinea pigs the ampullar endolymphatic potential was + 3.9 +/- 1.2 mV (n = 32), the Cl- activity 130 +/- 4.6 mM (n = 9), and the Na+ activity 18.4 +/- 4.4 mM (n = 20). After anoxia, the ampullar DC potential decreased rapidly and reversed its polarity within 5 min. It then decreased gradually for 60 min and increased afterwards to approximately zero. K+ activity decreased gradually after a latency of 10 min, whereas Na+ activity increased. During the gradual decrease of a negative ampullar endolymphatic potential, an increase in Na+ activity was observed. Thirty minutes after the intravenous injection of ethacrynic acid (100 mg/kg), the potential began to decrease, changed to a negative polarity, and approached a maximum negative level 100 min after the injection. The decrease in K+ activity corresponded to the reduction of potential whereas Na+ activity remained unchanged. The DC potential of the endolymphatic sac in normal guinea pigs was + 14.7 +/- 5.1 mV (n = 17). The Na+ concentration was 103.3 +/- 14.7 mM (n = 14) and the K+ concentration was 11.6 +/- 0.8 mM (n = 4). After anoxia, the DC potential decreased rapidly and approached 0 mV within 8 min. No negative potential could be observed. The Na+ concentration began to increase 2 min after anoxia and reached the extracellular Na+ concentration about 30 min later.(ABSTRACT TRUNCATED AT 250 WORDS)

We found changes in Ca++ activity and DC potential during the development of experimentally induced endolymphatic hydrops in guinea pigs. These findings indicate that there is some correlation between Ca++ activity and DC potential in the cochlear endolymph.

We measured Ca++ activity in the different parts of the endolymphatic space by using a double-barrelled electrode with calcium liquid ionic exchanger. In the region of the endolymphatic sac, Ca++ activity (4.7 X 10(-4) M) was much higher than in the cochlear duct (2.7 X 10(-5) M) and semicircular canal (2.6 X 10(-4) M). These findings suggest that Ca++ may also have a significant role in abnormal states.

The endolymphatic space of pigeons was studied by using double-barrelled electrodes with a potassium liquid ion exchanger. The K⁺ activity of the endolymph was 155 mM in the cochlea and 133 mM in the ampulla, respectively. Positive DC potential in the cochlea (+14.5 mV) was much lower than in guinea pigs (+80 mV) whereas in the ampulla of pigeons the DC potential (+7.4 mV) was 2 times higher than that of guinea pigs (+3.9 mV). General application of ethacrynic acid in pigeons induced a weak change in DC potential and no typical intercellular edema in the cochlea and ampulla. Local application of ethacrynic acid and ouabain in the cochlea and ampulla of pigeons induced a negative DC potential of between ––30 and ––40 mV. This negative DC potential was higher than the anoxia-induced negative potential. Short hypoxia during a drug-induced DC potential resulted in a decrease in DC potential above the diffusion potential. Below the diffusion potential additional hypoxia increased the DC potential independent of the cause of intoxication.

Ca++ concentrations and d.c. potential within the endolymphatic space of the cochlear duct and the semicircular canal following acute anoxia or ethacrynic acid intoxication (100 mg/kg i.v.) were measured by means of double-barrelled microelectrodes. Ionic calcium content and d.c. potential were found to change in a roughly biphasic fashion after either intervention. The maximal increase in Ca++ concentration coincided with the decline in the d.c. potential, which after a rapid decline finally reached and maintained negative voltages. This phenomenon was more pronounced in the cochlear part than in the semicircular canal. A model of calcium homeostasis is proposed in an attempt to reconcile the data presented with earlier evidence.