H. Togashi et al., CONSECUTIVE EVALUATION OF NITRIC-OXIDE PRODUCTION AFTER TRANSIENT CEREBRAL-ISCHEMIA IN THE RAT HIPPOCAMPUS USING IN-VIVO BRAIN MICRODIALYSIS, Neuroscience letters, 240(1), 1998, pp. 53-57
The time-course effects of transient cerebral ischemia on nitric oxide
(NO) formation in the rat hippocampus were evaluated by the consecuti
ve determination of oxidative NO metabolites (NO2- and NO3-), using br
ain microdialysis under the freely moving condition. Bilateral carotid
artery occlusion (CAO; 2-vessel occlusion, 2VO; 10 and 20 min) and co
mbined vertebral artery occlusion (4VO; 10 min) produced a transient i
ncrease in hippocampal NO2- and NO3- levels, according to the duration
and degree of ischemic insults. In addition, 4VO produced a gradual i
ncrease in hippocampal NO2- and NO3- levels over a 24 h period after r
eperfusion, which was abolished by an inducible NO synthase inhibitor,
aminoguanidine (10 mg/kg, intraperitoneally). These findings suggest
that the dynamic changes in oxidative NO metabolite levels reflect NO
production following transient cerebral ischemia, which is possibly me
diated in pari by an inducible NO synthase, in the rat hippocampus. (C
) 1998 Elsevier Science Ireland Ltd.