A physiologic technique was developed to measure endolymphatic cross-sectional area in vivo using tetramethylammonium (TMA) as a volume marker. The technique was evaluated in guinea pigs as an animal model. In the method, the cochlea was exposed surgically and TMA was injected into endolymph of the second turn at a constant rate by iontophoresis. The concentration of TMA was monitored during and after the injection using ion-selective electrodes. Cross-section estimates derived from the TMA concentration measurements were compared in normal animals and animals in which endolymphatic hydrops had been induced by ablation of the endolymphatic duct and sac 8 weeks earlier. The method demonstrated a mean increase in cross-sectional area of 258% in the hydropic group. Individually measured area values were compared with action potential threshold shifts and the magnitude of the endocochlear potential (EP). Hydropic animals typically showed an increase in threshold to 2 kHz stimuli and a decrease in EP. However, the degree of threshold shift or EP decrease did not correlate well with the degree of hydrops present.

Near normal levels of the endolymphatic potential (EP) of the guinea pig can be maintained for at least 3 h by perfusion of the anterior inferior cerebellar artery with “artificial blood,” composed of a perfluorochemical (FC 47) as oxygen carrier suspended in a physiological salt solution containing glucose [Wada et al., Laryngoscope, 1979, in press]. [We have now determined that glucose can be omitted from the medium, without deleterious effect upon the EP for periods exceeding 90 minutes. Apparently, the stria vascularis—the presumed generator of the EP—can maintain its function by relying upon its rich store of endogenous glycogen. However, by means of repeated hypoxic intervals, induced by interrupting perfusion, the glycolytic flux can be accelerated, thus expediting depletion of endogenous glycogen. Following several bouts of hypoxia, the substrate stores are reduced to the point that the EP starts declining at a constant rate of about 1 mV/min during glucose free perfusion. This decline can be reversed by applying a glucose (or succinate) containing medium. The rate and degree of recovery depend upon the glucose (or succinate) concentration in the medium. [Supported by NIH and NSF.]