| Project/Area Number |
09671192
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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 |
Embryonic/Neonatal medicine
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| Research Institution | Kobe University |
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Principal Investigator |
YONETANI Masahiko Kobe University, School of Medicine, Assistant, 医学部, 助手 (60221678)
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| Co-Investigator(Kenkyū-buntansha) |
相馬 収 神戸大学, 医学部附属病院, 助手 (70283893)
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| Project Period (FY) |
1997 – 1999
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| Project Status |
Completed (Fiscal Year 1999)
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| Budget Amount *help |
¥3,200,000 (Direct Cost: ¥3,200,000)
Fiscal Year 1999: ¥800,000 (Direct Cost: ¥800,000)
Fiscal Year 1998: ¥600,000 (Direct Cost: ¥600,000)
Fiscal Year 1997: ¥1,800,000 (Direct Cost: ¥1,800,000)
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| Keywords | Nitric oxide / Hypoglycemia / Striatum / 活性酸素 / 低血糖 / グルコース |
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| Research Abstract |
The present study tests the hypothesis that production of nitric oxide (NO) is affected by glucose deprivation and modulates cerebral blood flow (CBF) in developing rats striatum. The study was carried out in urethane-anesthetized 7-day-old (n=7) and14-day-old rats (n=6). We measured CBF in striatum by laser Doppler flowmetry and striatal NO level by No-selective amperometric microsensor. Microdialysis was used to monitor striatal extracellular glucose levels. Dialysate glucose was measured by HPLC system using ODS column linked directly to a glucose oxidase reactor. Following 2-hour stabilization after surgery, animal received an injection of regular insulin (50 IU/kg, i.p.). Extracellular glucose levels decreased significantly slower in 7-day-old rats compared to 14-day-old rats (p <0.01), but the trough levels which were reached by 180 min after injection were not statistically different (7.0±1.0% of baseline in 7 days old vs. 5.8±1.0% of baseline in 14 days old). CBF in striatum significantly increased from baseline as the striatal glucose level decreased, reaching 114±12% of baseline in 7-days-old rats and 121±23% of baseline in 14-day-old rats by 180 min after injection. However, NO level in striatum did not change markedly during insulin-induced hypoglycemia in all of the 7-day-old rats. Only one of six 14-day-old rats showed the marked increase in No production. Our results indicate that glucose deprivation induces cerebral hyperemia, but does not activate NO production. NO does not appears to mediate hypoglycemic hyperemia at least in immature rat striatum.
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