AI Article Synopsis
- The study investigated how nitric oxide (NO) production changes in the cochlea over 7 days after a short period of reduced blood flow (ischemia).
- Researchers used a selective inhibitor, aminoguanidine, to determine if NO production relies on the inducible nitric oxide synthase (iNOS) pathway.
- Results showed increased levels of oxidative NO metabolites on the first day and significant iNOS expression on days 1 and 4, indicating that transient ischemia leads to increased NO production primarily through the iNOS pathway.
Article Abstract
The present study was designed to elucidate the dynamic changes of nitric oxide (NO) production in the perilymph and to investigate the immunostaining for inducible nitric oxide synthase (iNOS) in the cochlea for 7 days after transient cochlear ischemia. Moreover, aminoguanidine, which is a selective iNOS inhibitor, was administrated immediately following ischemia and every 24h thereafter for 7 days to investigate whether the production of NO is dependent on the iNOS pathway. Significant increases in the oxidative NO metabolites, nitrite (NO(2)(-)) and nitrate (NO(3)(-)), were measured on day 1 using an in vivo microdialysis and on-line high performance liquid chromatography (HPLC) system. The immunostaining for iNOS was strongly expressed on days 1 and 4 and returned to normal on day 7 after the ischemia. The administration of aminoguanidine reduced the oxidative NO metabolites on day 1 and suppressed the expression of iNOS. These findings suggest that transient ischemia causes a remarkable increase in NO production in the perilymph, which might be attributable to the iNOS pathway.
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| http://dx.doi.org/10.1016/j.neulet.2005.08.038 | DOI Listing |
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