In vivo NMR study on the brain metabolism and biological active substabces under anesthesia and hypoxia
| Project/Area Number |
61480329
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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 |
麻酔学
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| Research Institution | Niigata University |
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Principal Investigator |
FUJIWARA Naoshi Niigata University School of Medicine, Assistant, 医学部, 助手 (70181419)
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| Co-Investigator(Kenkyū-buntansha) |
HASHIBA Masao Niigata University School of Medicine, Lecturer, 医学部附属病院, 講師
MATSUKI Michiko Niigata University School of Medicine, Associate Professor, 医学部, 助教授 (80018340)
YUASA Tatsuhiko Niigata University Brain Research Institute, Lecturer, 脳研究所, 講師 (10115090)
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| Project Period (FY) |
1986 – 1988
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| Project Status |
Completed (Fiscal Year 1988)
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| Budget Amount *help |
¥5,400,000 (Direct Cost: ¥5,400,000)
Fiscal Year 1988: ¥500,000 (Direct Cost: ¥500,000)
Fiscal Year 1987: ¥1,000,000 (Direct Cost: ¥1,000,000)
Fiscal Year 1986: ¥3,900,000 (Direct Cost: ¥3,900,000)
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| Keywords | NMR spectroscopy / Brain / Glucose metabolism / Energy charge / ^<13>C-glucose / Glutamate / 吸入麻酔薬 / MRS / エネルギー代謝 / グルコース代謝 / ^<13>C-glucose / glutamate isoflurane / In vivo ^<13>CNMR / ^<13>Cーグルコース / グルタミン酸 / 脳代謝 / 【^(13)C】-グルコース / 乳酸 |
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| Research Abstract |
The glucose metabolism and the changes in energy state and biological active substances in the brain during hypoxia and ischemia were investigated by ^<13>C, ^<31>P and ^1H NMR spectroscopy. Male Wistar rats were anesthetized with ketamine (50-75mg/kg i.p.) and ventilated mechanically with a mixture of 30% O_2, 69.5% N_2 and 0.5% halothane. [1-^<13>C]glucose (250Mg/kg) was infused twice through femoral vein at 10 min interval. [1-^<13>C]Glucose infusion gave apparent signals of C1 position in - and - anomers of [1-^<13>C]glucose at 92.7 and 96.7 ppm, respectively. Signals of C2, C3 and C4 positions in glutamate (glu) also appeared at 55, 27 and 34 ppm, respectively. The intensity of glu-C2 and glu-C3 signals increased later than that of glu-C4. The time lag between the glu signals may reflect the turnover rate of the TCA cycle. In the hypoxic experiments, O_2 concentration in the inspiratory gas was reduced to 6-7% (93-94% N_2). During hypoxia, the signal of lactate-^<13>C3 appeared at
… More
21 ppm and increased, and the -glucose signal diminished, whereas the -glucose signal kept its intensity. The difference in changes of the signal intensity between -and -glucose suggests that -glucose is consumed more than -glucose in the hypoxic brain. Under similar hypoxic condition, the ^<31>P signal intensity of creatine phosphate (pcr) decreased by 27% but the signal of ATP was unchanged in 30min. In the ^1H spectra, increase in the lactate-CH_3 signal also suggests the enhancement of anaerobic glycolisis in hypoxic brain.
Mongolian gerbils were anesthetized with pentobarbital (35mg/kg, i.p.). A bolus of [1-^<13>C]-glucose (500mg/kg) was injected into femoral vein. Forbrain ischemia by bilateral common carotid occlusion was induced 15min after the glucose injection. In the ischemic brain, signals of both - and -glucose rapidly disappeared, and the signal of lactate- ^<13>C3 became prominent. The glutamate signals did not appeare during ischemia and even in post-ischemia. In the ^<31>P spectra, signals of both Pcr and ATP disappeared. Thereford, not only energy charge but also glutamate synthesis may be deperssed in the ischemic brain. Less
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Report
(4 results)
Research Products
(15 results)
