| Project/Area Number |
05454345
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| Research Category |
Grant-in-Aid for General Scientific Research (B)
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| Allocation Type | Single-year Grants |
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| Research Field |
Embryonic/Neonatal medicine
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| Research Institution | Kobe University |
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Principal Investigator |
NAKAMURA Hajime Kobe University, School of Medicine, Professor, 医学部, 教授 (40030978)
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| Co-Investigator(Kenkyū-buntansha) |
SANO Kimihiko Kobe University, School of Medicine, Lecturer, 医学部・附属病院, 講師 (40205993)
TAKADA Satoshi Kobe University, School of Medicine, Assistant, 医学部, 助手 (10216658)
UETANI Yoshiyuki Kobe University, School of Medicine, Lecturer, 医学部, 講師 (40168620)
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| Project Period (FY) |
1993 – 1994
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| Project Status |
Completed (Fiscal Year 1994)
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| Budget Amount *help |
¥6,600,000 (Direct Cost: ¥6,600,000)
Fiscal Year 1994: ¥1,900,000 (Direct Cost: ¥1,900,000)
Fiscal Year 1993: ¥4,700,000 (Direct Cost: ¥4,700,000)
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| Keywords | Newborn / Hypoxic brain damage / Nerotrophic factors / Nitric oxide / Dopamine / 脳虚血 / マイクロダイアリシス / アセチルコリン |
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| Research Abstract |
The present study was performed to investigate the role of nitric oxide (NO), one of the neurophic factors for the repair from the ischemic brain damage by the in vivo microdialysis technique.
Method : 7-day-old Sprague-Dawley rats were anesthetized with urethane, and microdialysis probe (CMA11) was implanted into the striatum, and the probe was conditioned by the Ringer's solution. The animals were divided into three groups : Control group, L-arginine (NO synthetic drug) administered group, and N-nitro-L-arginine methyl ester (L-NAME) (NO synthase inhibitor) administered group. After insertion of probe, 2-h period was allowed for stabilization. They were exposed to 8% O2 for 60 minutes, and followed reoxygenation with 21% O2. Either L-arginine or L-Name at a dose of 100 ug/dl were injected to the striatum by a probe from 30 minutes before the onset of hypoxia to the end of experiment. Extracellular dopamine and the metabolites ; Dihydroxy-phenylacetic acid (DOPAC) and homovanillic acid (HVA) were determined by the HPLC-electro-chemical technique.
Results : The dopamine concentration in control group was increased to 2.4 times of the level before the hypoxia at the 60 minutes of hypoxia, and recovered to the baseline by the reoxugenation. The increment of the dopamine concentration in the L-arginine group was 2.3 times of the baseline, as highly as the controls, and that in the L-NAME group was as low as 1.4 times of the baseline. The extracellular dopamine metabolites, DOPAC and HVA,were decreased by the hypoxia. These results suggest that inhibition of NO systhesis plays a role for the prevention from the brain injury due to hypoxia.
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