This study was designed to evaluate the role of endogenous nitric oxide (NO
) in focal microcirculation disorder of the guinea pig cochlea. Focal micro
circulation disorder was induced by a photochemical reaction at the lateral
wall of the second cochlear turn. Saline or No-nitro-L-arginine methyl est
er (L-NAME) was administered before the onset of photochemical reaction. Co
chlear 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 activitie
s were measured by radioenzymeassay. In the saline pretreatment group, CBF
was significantly decreased to 58.8 +/- 4.4% of the baseline at the ischemi
c core 30 min after the onset of photochemical reaction (P < 0.01), while C
BF showed no significant change at the ischemic border zone. In the L-NAME
pretreatment group, CBF was significantly decreased not only at the focal l
esion (48.3 +/- 6.5%, P < 0.01), but also at the ischemic border zone (apic
al, 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 format
ion of endogenous NO plays a key role in the maintenance of CBF in acute fo
cal cochlear microcirculation disorder. (C) 2001 Elsevier Science B.V. All
rights reserved.