| Project/Area Number |
11680833
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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 |
Biomedical engineering/Biological material science
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| Research Institution | ASAHIKAWA MEDICAL COLLEGE |
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Principal Investigator |
TANAKA Kunio Asahikawa Medical College Associate Professor, 医学部, 助教授 (20041840)
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| Co-Investigator(Kenkyū-buntansha) |
NAKAI Hirofumi Asahikawa Medical College Associate Professor, 医学部, 助教授 (20142820)
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| Project Period (FY) |
1999 – 2000
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| Project Status |
Completed (Fiscal Year 2000)
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| Budget Amount *help |
¥3,800,000 (Direct Cost: ¥3,800,000)
Fiscal Year 2000: ¥1,100,000 (Direct Cost: ¥1,100,000)
Fiscal Year 1999: ¥2,700,000 (Direct Cost: ¥2,700,000)
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| Keywords | 31P-MRS / phosphate metabolism / mild hypothermia / brain protection / ATP / phosphocreatine / inorganic phosphate / forebrain ischemia / 脳内リンエネルギー代謝 |
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| Research Abstract |
The purpose of this study was to clarify the mechanism of the effect of the brain protection due to mild hypothermia, from the view point of the phosphate metabolism by using 31P-MRS.
1) The hippocampal temperature was lower than the rectal temperature in both groups. The hippocampal and rectal temparature rapidly fell following the ischemia in both groups. After the reperfusion, the hippocampal temperature returned to the pre-ischemic level within 16 min and the rectal temperature also returned within 30 min.
2) Following the induction of ischemia, ATP and creatine phosphate (PCr) rapidly decreased to 20-30% of the control level in both groups. After the reperfusion, ATP and PCr levels rapidly recovered to 90% of the control level in mild hypothermic group. In normothermic group, the recovery of ATP and PCr levels was significantly slower than that in mild hypothermic group, and the recovered level was 80% of the control level. Inorganic phosphate (Pi) levels in both groups rapidly increased following the ischemia. After the reperfusion, Pi level rapidly recovered to its initial level in mild hypothermic group. Significant delay and the reduction of the recovered level in Pi were observed in normothermic group.
3) In both groups, intracellular pH decreased to the same level following the ischemia. After the reperfusion, it returned faster to the control level in mild hypothermic group compared to that in normothermic group.
4) Significant differences in the extent of ischemic damage were not observed in each group by using autoradiography.
4) The neuronal damage at hippocampus and cerebral cortex was greater in normothermic group than that in mild hypothermic group.
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