Abstract
Nitric oxide (NO) is considered to be associated with the pathogenesis of cerebral ischemic injury. In the present study, NO production was continuously monitored employing in vivo microdialysis. A microdialysis probe was inserted into the striatum. Levels of the major NO metabolite, NO2- in the dialysate were determined using the Griess reaction. Rats were subjected to global cerebral ischemia produced by occlusion of both common carotid arteries together with induced hypotension. Cerebral ischemia induced a decrease in NO production, which was interrupted by a transient increase in NO synthesis. This increment was abolished in the presence of a NO synthase inhibitor, N(G)-nitro-L-arginine methyl ester (L-NAME), suggesting that NO synthase activity is transiently activated during ischemia. Following reperfusion, NO synthesis was enhanced. To our knowledge, this is the first report concerning the continuous temporal profile of NO production during global cerebral ischemia and reperfusion.
| Original language | English |
|---|---|
| Pages (from-to) | 86-90 |
| Number of pages | 5 |
| Journal | Brain Research |
| Volume | 734 |
| Issue number | 1-2 |
| DOIs | |
| Publication status | Published - 1996 Sep 23 |
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Keywords
- Cerebral ischemia
- Griess reaction
- Microdialysis, in vivo
- Nitric oxide
- Nitrite
- Striatum
ASJC Scopus subject areas
- Neuroscience(all)
Cite this
Brain nitrite production during global ischemia and reperfusion : An in vivo microdialysis study. / Shibata, Mamoru; Araki, Nobuo; Hamada, Junichi; Sasaki, Takahiro; Shimazu, Kunio; Fukuuchi, Yasuo.
In: Brain Research, Vol. 734, No. 1-2, 23.09.1996, p. 86-90.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Brain nitrite production during global ischemia and reperfusion
T2 - An in vivo microdialysis study
AU - Shibata, Mamoru
AU - Araki, Nobuo
AU - Hamada, Junichi
AU - Sasaki, Takahiro
AU - Shimazu, Kunio
AU - Fukuuchi, Yasuo
PY - 1996/9/23
Y1 - 1996/9/23
N2 - Nitric oxide (NO) is considered to be associated with the pathogenesis of cerebral ischemic injury. In the present study, NO production was continuously monitored employing in vivo microdialysis. A microdialysis probe was inserted into the striatum. Levels of the major NO metabolite, NO2- in the dialysate were determined using the Griess reaction. Rats were subjected to global cerebral ischemia produced by occlusion of both common carotid arteries together with induced hypotension. Cerebral ischemia induced a decrease in NO production, which was interrupted by a transient increase in NO synthesis. This increment was abolished in the presence of a NO synthase inhibitor, N(G)-nitro-L-arginine methyl ester (L-NAME), suggesting that NO synthase activity is transiently activated during ischemia. Following reperfusion, NO synthesis was enhanced. To our knowledge, this is the first report concerning the continuous temporal profile of NO production during global cerebral ischemia and reperfusion.
AB - Nitric oxide (NO) is considered to be associated with the pathogenesis of cerebral ischemic injury. In the present study, NO production was continuously monitored employing in vivo microdialysis. A microdialysis probe was inserted into the striatum. Levels of the major NO metabolite, NO2- in the dialysate were determined using the Griess reaction. Rats were subjected to global cerebral ischemia produced by occlusion of both common carotid arteries together with induced hypotension. Cerebral ischemia induced a decrease in NO production, which was interrupted by a transient increase in NO synthesis. This increment was abolished in the presence of a NO synthase inhibitor, N(G)-nitro-L-arginine methyl ester (L-NAME), suggesting that NO synthase activity is transiently activated during ischemia. Following reperfusion, NO synthesis was enhanced. To our knowledge, this is the first report concerning the continuous temporal profile of NO production during global cerebral ischemia and reperfusion.
KW - Cerebral ischemia
KW - Griess reaction
KW - Microdialysis, in vivo
KW - Nitric oxide
KW - Nitrite
KW - Striatum
UR - http://www.scopus.com/inward/record.url?scp=0030599172&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=0030599172&partnerID=8YFLogxK
U2 - 10.1016/0006-8993(96)00617-8
DO - 10.1016/0006-8993(96)00617-8
M3 - Article
C2 - 8896812
AN - SCOPUS:0030599172
VL - 734
SP - 86
EP - 90
JO - Brain Research
JF - Brain Research
SN - 0006-8993
IS - 1-2
ER -