Objective: To investigate the effect of acoustic overstimulation on concentrations of cations in cochlear endolymph and analyze the relationship between the ionic changes in endolymph and the hearing loss.
Methods: The endocochlear potentials (EP), K+, Na+ and Ca2+ concentration in cochlear endolymph were examined in vivo for normal and 167 +/- 2 dB SPL impulse noise exposed groups of guinea pig bored on time course by means of double-barreled ion-selective microelectrodes. Brain stem auditory evoked potential (BAEP) was used to evaluate the auditory function. Ca(2+)-ATPase activity was demonstrated cytochemically in the lateral cochlear wall as induced by Ando et al with slight modification.
Results: The K+ and Ca2+ concentration exhibited significant changes in 8-hour groups (P < 0.05 for K+ and P < 0.01 for Ca2+). Then the K+ concentration was eventually resumed to the initial levels in accordance with the EP recovery in 7 days, while during the same period Ca2+ concentration was always significantly higher than that in control group (P < 0.01). The BAEP threshold shifts were correlated well with changes in ionic concentrations, especially Ca2+ (P < 0.001), in the endolymph induced by acoustic trauma. Although the normal positive EP was observed 7 days after noise exposure, the function of the vascular stria was not completely restored as revealed by the fact that the Ca(2+)-ATPase was diffused to the apical membrane surface.
Conclusions: Endolymph compartment intrinsic mechanism for maintaining ionic composition is seriously deteriorated after high impulse noise stimulation. The changes of the unique environment of endolymph may play an important role in the mechanism of sensorineural hearing loss induced by acoustic trauma.