| Project/Area Number |
05670584
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| Research Category |
Grant-in-Aid for General Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Research Field |
Neurology
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| Research Institution | NATIONAL CARDIOVASCULAR CENTER RESEARCH INSTITUTE |
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Principal Investigator |
NARITOMI Hiroaki National Cardiovascular Center Research Institute, Department of Cardiovascular Dynamics, Laboratory Director, 循環動態機能部, 室長 (60132932)
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| Co-Investigator(Kenkyū-buntansha) |
KANASHIRO Masaru National Cardiovascular Center Research Institute, Department of Biomedical Engi, 生体工学部, 室長 (10132929)
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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 |
¥2,200,000 (Direct Cost: ¥2,200,000)
Fiscal Year 1994: ¥900,000 (Direct Cost: ¥900,000)
Fiscal Year 1993: ¥1,300,000 (Direct Cost: ¥1,300,000)
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| Keywords | cerebral ischemia / heat-shock protein / ischemic tolerance / astrocyte / energymetabolism / 31P-NMR spectroscopy / hyppocampus / delayd neuronal death / エネルギー代謝 / ^<31>P NMRスペクトロスコピー / 遅発性神経細胞壊死 |
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| Research Abstract |
In order to clarify wehther focal ischemic insults can cause ischemic tolerance in neurons in the surrounding areas, immunohistochemical and 31p-NMR spectroscopic studes were undertaken in mongolian gerbils. Right cortical infarction was induced by skull magnet-minute magnetite particle intravenous injection methods or middle cerebral artery occlusion. The infarction was found to cause no induction of HSP70 mRNA in infarcted areas and the adjacent hippocampus. Immunohistochemical studies showed GFAP-positive astrocytes accumulation in the infarcted area and the adjacent hippocampal CA1 sectros at 3 and 7 days after infarction. 5-min forebrain ischemia conducted at 1,3 or 7 days after infarction caused diffuse neuronal death in the non-infarcted side CA1 sectors. However, 5 min forebrain ischemia at 3 days after infarction brought about small number of neuronal death in the infarcted side CA1 sector. This ischemic tolerance was most remarkable in the CA1 sector adjacent the infarction. Less prominent ischemic tolerance was observed in a group with 5-min ischemia at 1 day after infarction. Yet, no such tolerance was observed in agroup with 5 min ischemia at 7 days after infarction. 31P-NMR studies indicated that forebrain ischemia caused severe energy disturbance irrespectively of existence of infarction. The results suggest that during several days after focal infarction, neurons in the surrounding areas may show ischemic tolerance. This tolerance is not attributable to induction of heat-shock protein or improvement of energy failure. Presumably, reactive atrocytes may exert protective effects on the adjacent neurons.
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