The effects of ethacrynic acid upon EP and its mechanism of action (Japanese)

The influence of ethacrynic acid (EA) on the endocochlear potential (EP) and the high energy compounds ATP and phosphocreatine in the stria vascularis was studied at various conditions such as induced ischemia. When EP was reduced at the most by EA, no major changes occur in the high energy compounds in contrast with the analogous situation in anoxia or cyanide intoxication. When EA intoxicated ears were exposed to ischemia at the mostly reduced level, the levels of the high energy compounds were maintained much longer than that in untreated ears, and the decline of EP was much slower with the initial rate of change roughly proportional to the preischemic level of EP. This initial decline of EP by EA is considered to be due to the reduction of positive electrogenic K⁺ secretion potential by the inhibition of energy utilizing mechanism mediated by Na⁺K⁺ ATPase system. When this maximally reduced level was lower than about -15mV, this negativity of the potential was decreased by ischemia. The possible mechanism of this phenomenon is discussed. When the ischemia was made in the slow recovery stage, the decline rate of the potential was far slower than that at the maximally reduced level. It is considered that the reduction of positive K⁺ secretion potential, in this stage, is already accompanied by the change of the diffusion potential due to the change of the membrane permeability in the cochlear duct and the ionic composition of the endolymph.