TY - JOUR
T1 - Electron paramagnetic resonance study on nitric oxide production during brain focal ischemia and reperfusion in the rat
AU - Sato, Shinya
AU - Tominaga, Teiji
AU - Ohnishi, Tomoko
AU - Ohnishi, S. Tsuyoshi
N1 - Funding Information:
The authors are grateful to Prof. Takashi Yoshi-moto, Chairman of the Division of Neurosurgery, Institute of Brain Diseases, Tohoku University School of Medicine, for his encouragement. Thanks are also due to Dr. Larry Keefer of the Chemistry Section at NCI for his valuable suggestions. The work was supported by NIH grants NS30186 to S.T.O. and GM30736 to T.O.
PY - 1994/5/30
Y1 - 1994/5/30
N2 - The production of nitric oxide (NO) during brain focal ischemia and reperfusion was using diethyldithiocarbamate (DETC)/ Fe-citrate, NO trapping reagents, and electron paramagnetic resonance spectroscopy. The NO production is potentiated after 5 min of ischemia, and is continued during 60 min of ischemia. During the reperfusion period after 60 min of ischemia, NO was also produced. However, its production during reperfusion was not observed when the ischemia time was less than 15 min. The NO signal during reperfusion after 60 min of ischemia decreased after 15 min of reperfusion. These results suggest that NO production during ischemia is a physiological reaction for increasing cerebral blood flow, while NO production during reperfusion may be related to cellular damage.
AB - The production of nitric oxide (NO) during brain focal ischemia and reperfusion was using diethyldithiocarbamate (DETC)/ Fe-citrate, NO trapping reagents, and electron paramagnetic resonance spectroscopy. The NO production is potentiated after 5 min of ischemia, and is continued during 60 min of ischemia. During the reperfusion period after 60 min of ischemia, NO was also produced. However, its production during reperfusion was not observed when the ischemia time was less than 15 min. The NO signal during reperfusion after 60 min of ischemia decreased after 15 min of reperfusion. These results suggest that NO production during ischemia is a physiological reaction for increasing cerebral blood flow, while NO production during reperfusion may be related to cellular damage.
KW - Brain ischemia
KW - Cerebral blood flow
KW - Diethydithiocarbamate
KW - Electron paramagnetic resonance
KW - Nitric oxide
KW - Reperfusion
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U2 - 10.1016/0006-8993(94)91402-8
DO - 10.1016/0006-8993(94)91402-8
M3 - Article
C2 - 8069708
AN - SCOPUS:0028238555
VL - 647
SP - 91
EP - 96
JO - Molecular Brain Research
JF - Molecular Brain Research
SN - 0006-8993
IS - 1
ER -