Consecutive evaluation of nitric oxide production after transient cerebral ischemia in the rat hippocampus using in vivo brain microdialysis.
The time-course effects of transient cerebral ischemia on nitric oxide (NO) formation in the rat hippocampus were evaluated by the consecutive determination of oxidative NO metabolites (NO2- and NO3-), using brain microdialysis under the freely moving condition. Bilateral carotid artery occlusion (CAO; 2-vessel occlusion, 2VO; 10 and 20 min) and combined vertebral artery occlusion (4VO; 10 min) produced a transient increase in hippocampal NO2- and NO3- levels, according to the duration and degree of ischemic insults. In addition, 4VO produced a gradual increase in hippocampal NO2- and NO3- levels over a 24 h period after reperfusion, 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 mediated in part by an inducible NO synthase, in the rat hippocampus.
Togashi
H
H
First Department of Pharmacology, Hokkaido University School of Medicine, Sapporo, Japan. thiro@med.hokudai.ac.jp
Mori
K
K
Ueno
K
K
Matsumoto
M
M
Suda
N
N
Saito
H
H
Yoshioka
M
M
D000818:Animals; D002545:Brain Ischemia / Q000378:metabolism* / Q000503:physiopathology; D015314:Dialysis Solutions / Q000378:metabolism; D006624:Hippocampus / Q000098:blood supply / Q000378:metabolism*; D008297:Male; D017551:Microdialysis; D009569:Nitric Oxide / Q000096:biosynthesis* / Q000378:metabolism; D051381:Rats; D017208:Rats, Wistar; D015427:Reperfusion Injury / Q000378:metabolism
D015314:Dialysis Solutions; D009569:Nitric Oxide