| Project/Area Number |
09671193
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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 | Kagawa Medical University |
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Principal Investigator |
ONISHI Shoji Kagawa Medical School Professor, 医学部, 教授 (40080014)
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| Co-Investigator(Kenkyū-buntansha) |
IMAI Tadashi Kagawa Medical School Instructor, 医学部, 助手 (60176477)
ISOBE Kenichi Kagawa Medical School Assistant Professor, 医学部・附属病院, 講師 (00159815)
ITOH Susumu Kagawa Medical School Assistant Professor, 医学部, 講師 (80145052)
KAWADA Kou Kagawa Medical School Instructor, 医学部・附属病院, 助手 (40284369)
KUSAKA Takashi Kagawa Medical School Instructor, 医学部・附属病院, 助手 (50274288)
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| Project Period (FY) |
1997 – 1998
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| Project Status |
Completed (Fiscal Year 1998)
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| Budget Amount *help |
¥3,600,000 (Direct Cost: ¥3,600,000)
Fiscal Year 1998: ¥900,000 (Direct Cost: ¥900,000)
Fiscal Year 1997: ¥2,700,000 (Direct Cost: ¥2,700,000)
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| Keywords | redox state of cytochrome c oxidase / phosphocreatine / inorganic phosphate / insulin-indeced hypoglycemia / newborn piglet brain / ィイD131ィエD1P-magnetic resonance spectroscopy / cerebral oxygenation / full-spectrum near infrared spectroscopy / piglet / 近赤外分光測定 / チトクロームCオキシターゼ / 低血糖症 / 脳内ヘモグロビン酸素飽和度 / 脳血液量 / ^<31>P-核磁気共鳴スペクトロスコピー |
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| Research Abstract |
Glucose is the major substrate for the cerebral energy metabolism, and brain damage can result when the glucose supply is severely restricted. The purpose of the present study was to investigate the relation between the redox state of cytochrome c oxidase and phosphocreatine/inorganic phosphate (PCr/Pi) during insulin-induced hypoglycemia in the newborn piglet brain. We simultaneously measured the cerebral energy metabolism by ィイD131ィエD1P-Resonance Spectroscopy (ィイD131ィエD1P-MRS) and the cerebral oxygenation by full-spectrum near infrared spectroscopy (fsNIRS). Five newborn piglets were studied ; within 24 hours after birth. Hypoglycemia was induced by bolus injection of rapid insulin.
Total Hb rose slightly, under insulin load, when there was a gradual decrease in blood glucose. While blood glucose remained above 10 mg/dl, the oxidized form of cytochrome c oxidase remained nearly unchanged or rose slightly. When blood glucose was reduced to a level lower than 10 mg/dl, the oxidized form of cytochrome c oxidase fell rapidly.
Moreover, PCr/Pi remained above 1.2, while the oxidized form of cytochrome c oxidase was almost constant between 55-70%. However, below 1.2, the oxidized form of cytochrome c oxidase decreased linearly with PCr/Pi. Furthermore, the oxidized form of cytochrome c oxidase during hypoglycemic loading was only slightly lower than the oxidized form of cytochrome c oxidase that had been reduced during hypoxic loading.
The administration of glucose caused the oxidized form of cytochrome c oxidase to recover to the prevalue in about 30 mm, whereas the recovery of PCr/Pi was slower.
The above results serve to explain that prolonged severe hypoglycemia causes the depletion of ATP in brain cells and in turn an insufficient amount of energy for the maintenance of microstructures within the cells, thus producing a strain on the subunits of cytochrome c oxidase. However, further detailed study is necessary.
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