Role of nitric oxide in focal microcirculation disorder of guinea pig cochlea

This study was designed to evaluate the role of endogenous nitric oxide (NO) in focal microcirculation disorder of the guinea pig cochlea. Focal microcirculation disorder was induced by a photochemical reaction at the lateral wall of the second cochlear turn. Saline or N omega-nitro-L-arginine methyl ester (L-NAME) was administered before the onset of photochemical reaction. Cochlear blood flow (CBF) was measured at the focal lesion (ischemic core), 1 mm from the lesion in the apical and basal direction (ischemic border zone) by using a novel non-contact laser blood flowmeter. NO synthase activities were measured by radioenzymeassay. In the saline pretreatment group, CBF was significantly decreased to 58.8+/-4.4% of the baseline at the ischemic core 30 min after the onset of photochemical reaction (P<0.01), while CBF showed no significant change at the ischemic border zone. In the L-NAME pretreatment group, CBF was significantly decreased not only at the focal lesion (48.3+/-6.5%, P<0.01), but also at the ischemic border zone (apical, 49.3+/-2.3%, P<0.05; basal, 58.7+/-7.1%, P<0.05, respectively). NO synthase III activity of cochlea was increased significantly (P<0.01) 15 min after microcirculation disorder. These findings suggest that formation of endogenous NO plays a key role in the maintenance of CBF in acute focal cochlear microcirculation disorder.