We have established a new animal model for investigating the mechanism of hearing loss caused by microcirculation disorder by using a photochemical reaction between the systemic injection of Rose Bengal (RB) and green light illumination to the guinea pig cochlea. Degeneration of the stria vascularis (SV), whose length was 760 μm on average, and increase of diameter in the capillary of the SV were observed. The SV seems to be sensitive for the photochemical reaction. The histological findings in the photochemically injured lesion of SV supported the damage caused by active oxygen species. In physiological studies, the compound action potentials (CAP) and endocochlear potential (EP) and cochlear blood flow (CBF) were significantly affected by the interruption of segmental blood supply in the cochlea. The region between the double lesions in the SV induced hair cell loss, but reversible reduction of EP. Pretreatment with the L-NAME (Nω-nitro-L-arginine methyl ester) decreased the CBF significantly not only at the focal lesion, but also at the ischemic border zone. NO synthase III activity of cochlea was increased significantly. These findings suggest that formation of endogenous NO plays a key role in the maintenance of CBF in acute focal cochlear microcirculation disorder. The present findings will be of use in explaining some cases of sensorineural hearing loss for which the causes are yet unknown.
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