Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
. 1986;243(3):180-2.
doi: 10.1007/BF00470616.

An experimental study using sodium salicylate to reduce cochlear changes induced by furosemide

An experimental study using sodium salicylate to reduce cochlear changes induced by furosemide

L P Rybak et al. Arch Otorhinolaryngol. 1986.

Abstract

Furosemide is a loop diuretic which has been found to be ototoxic in humans and experimental animals. The ototoxic effects seem to be directed primarily towards the stria vascularis, since its shrinkage and extracellular edema have been observed in correlation with electrophysiologic changes. The present study was designed to examine the interaction of sodium salicylate and furosemide on the cochlear microstructures. Chinchillas weighing 400-600 g were used in all tests performed. The endocochlear potential (EP) was monitored continuously through a microelectrode inserted through the basilar membrane. A control group of animals was injected with 0.5 ml saline intravenously (IV) 30 min before 25 mg/kg furosemide was given. The experimental group of animals was injected with 50 mg/kg sodium salicylate IV 30 min before 25 mg/kg furosemide. The control animals were found to have a mean decrease in EP of 61.1 +/- 7.0 mV. In contrast, the experimental group had very little alteration of the EP following furosemide injection (18.7 +/- 3.9 mV). These findings suggest that sodium salicylate markedly reduces the ototoxic effect of furosemide. This effect may be mediated by an alteration of local or systemic prostaglandin metabolism, or may be due to inhibition of organic acid uptake in the cochlea.

PubMed Disclaimer

References

    1. Pharmacol Rev. 1974 Mar;26(1):33-67 - PubMed
    1. J Pharmacol Exp Ther. 1984 Sep;230(3):706-9 - PubMed
    1. Laryngoscope. 1978 Jan;88(1 Pt 1):12-37 - PubMed
    1. Laryngoscope. 1985 Sep;95(9 Pt 2 Suppl 38):1-14 - PubMed
    1. Bull Johns Hopkins Hosp. 1959 Nov;105:284-97 - PubMed

Publication types