| Summary: | <p>Abstract</p> <p>Background</p> <p>The permanent hearing loss following exposure to intense noise can be due either to mechanical structural damage (tearing) caused directly by the noise or to metabolic (biochemical) damage resulting from the elevated levels of free radicals released during transduction of the sound overstimulation. Drugs which depress active cochlear mechanics (e.g. furosemide and salicylic acid) or anti-oxidants (which counteract the free radicals) are effective in reducing the threshold shift (TS) following broadband continuous noise. This study was designed to determine whether furosemide can reduce the TS following exposure to impulse noise, similar to its action with continuous broadband noise.</p> <p>Methods</p> <p>Shortly after furosemide injection, mice were exposed to <it>simulated </it>M16 rifle impulse noise produced by different loudspeakers and amplifiers in different exposure settings and, in other experiments, also to <it>actual </it>M16 rifle shots.</p> <p>Results</p> <p>Depending on the paradigm, the <it>simulated </it>noises either did not produce a TS, or the TS was reduced by furosemide. The drug was not effective in reducing TS resulting from <it>actual </it>impulse noise.</p> <p>Conclusion</p> <p><it>Simulated </it>M16 rifle impulse noise may not truly replicate the rapid rise time and very high intensity of <it>actual </it>rifle shots so that the TS following exposure to such noise can be reduced by these drugs. On the other hand, <it>actual </it>M16 impulse noise probably causes direct (frank) mechanical damage, which is not reduced by these drugs.</p>
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