The effects of indomethacin on inner ear fluids and morphology

Metabolic disturbances may affect inner ear fluid homeostasis in various ways. The membrane sodium-potassium pump must play a role in this homeostasis, and as this pump derives energy from A.T.P. it may also depend somewhat on the presence of prostaglandins, through their stimulatory effect on the adenylate cyclase system. Salicylates suppress prostaglandins; and Indomethacin is even more potent in this respect. Could the temporary ototoxic effects of salicylates and Indomethacin be due to prostaglandin suppression? Further, could energy system problems involving prostaglandins be related to the development of endolymphatic hydrops? These questions prompted this study. Sublethal doses of Indomethacin were given to 14 guinea pigs in order to maximally suppress prostaglandins. Samples of perilymph and endolymph were analyzed for sodium and potassium concentrations and compared to normal controls. No significant differences were found in either acute (two to 24 hour) or chronic (three week) experiments. Light microscopic examination of serially sectioned cochleae in similarly treated animals showed, in a few cases, somewhat questionable distension of Reissner's membrane. Electron microscopy or the organ of Corti did not demonstrate any abnormalities. The study suggests that Indomethacin does not produce significant inner ear electrolyte shifts or endolymphatic distension, at least over the short term.