| Project/Area Number |
12671493
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Anesthesiology/Resuscitation studies
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| Research Institution | Fukushima Medical University |
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Principal Investigator |
OTSUKI Manabu School of Medicine, Fukushima Medical University, Assistant professor, 医学部, 助教授 (70233195)
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| Co-Investigator(Kenkyū-buntansha) |
MURAKAWA Masahiro School of Medicine, Fukushima Medical University, Professor, 医学部, 教授 (90182112)
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| Project Period (FY) |
2000 – 2001
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| Project Status |
Completed (Fiscal Year 2001)
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| Budget Amount *help |
¥2,400,000 (Direct Cost: ¥2,400,000)
Fiscal Year 2001: ¥1,100,000 (Direct Cost: ¥1,100,000)
Fiscal Year 2000: ¥1,300,000 (Direct Cost: ¥1,300,000)
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| Keywords | carbon monoxide / hypoxia / neuronal cell damage / microdialysis / acetylcholine / amino acid / グルタミン酸 / 脳内アセチルコリン |
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| Research Abstract |
To investigate the effect of hypoxia or carbon monoxide exposure on the neuronal cell damage, the in-vivo extracellular release of acetylcholine and amino acids from frontal cortex of rats was measured by intracerebral microdialysis. Histopathological studies were also performed to evaluate the neuronal cell damage. Young male wistar rats by inserting a microdialysis probe into the frontal cortex were placed in a small plastic chamber and exposed to mixed gas of 5% O2 and 95% N2 or CO at 2000 ppm in air for 60 minutes. Acetylcholine and amino acids were measured using HPLC-ECD and the dialysate was collected every 15 minutes.
Hypoxia increased acetylcholine concentration after 30 minutes of inhalation with no significance. CO exposures increased acetylcholine concentration significantly during exposure and the late period (150 min) of reoxygenation. Glutamate concentration was increased during 30 min of hypoxia and the early period (15 min) of reoxygenation, but no significance. On the other hand, CO exposures increased glutamate concentration during the late period (45 min) of hypoxia and the late period of reoxygenation. CO exposures also increased glutamine, asparagine, arginine, glycine, alanine and threonine concentrations and these alternations were significant compared to those of hypoxia. Hypoxia and CO exposures increased GABA concentration similarly after 30 min of inhalation. Taurine concentration was decreased during inhalation of both gas, but hypoxia affected this decline more than CO. A mild morphological alternation was observed in the hipocampal CA3 and CA4 regions, but no such a change was recognized in the CA1 and cerebral cortex. There were no defference between two inhalation groups.
It is suggest that CO exposure is more harmful to neuronal cells than hypoxia alone because of affecting neurotransmitters release more than hypoxia does.
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