| Project/Area Number |
61480304
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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 |
Cerebral neurosurgery
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| Research Institution | TOHOKU UNIVERSITY |
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Principal Investigator |
YOSHIMOTO Takashi Tokoku University School of Medicine (Associate Professor), 医学部(脳神経外科), 助教授 (50091765)
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| Co-Investigator(Kenkyū-buntansha) |
KAMEYAMA Motonobu Tohoku University School of Medicine, 医学部(脳神経外科), 助手 (70169647)
MIZOI Kazuo Tohoku University School of Medicine (KAWAZOE,Yosh), 医学部(脳神経外科), 助手 (70157519)
IDO Tatsuo Cyric, Tohoku University (Professor), サンクロトロンラジオアイソトープセンター(RI製造), 教授 (80134063)
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| Project Period (FY) |
1986 – 1987
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| Project Status |
Completed (Fiscal Year 1987)
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| Budget Amount *help |
¥6,300,000 (Direct Cost: ¥6,300,000)
Fiscal Year 1987: ¥500,000 (Direct Cost: ¥500,000)
Fiscal Year 1986: ¥5,800,000 (Direct Cost: ¥5,800,000)
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| Keywords | Complete forebrain ischemia / reperfusion / cerebral blod flow / glucose metabolism / amino acid metabolism / No-reflow phenomenone / Mannitol / マンニットール / 脳虚血 / グルコース代謝 / アミノ酸代謝 / 脳血流量 / 多重標識オートラジオグラフィー / 多角的代謝動態 |
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| Research Abstract |
An experimental model of rat forebrain ischemia regulated with perfusion method was created. The preparation mainly consists of the occlusion of bilateral externel earotid, pterygopalatine arteries and basilar artery, then the brain is perfused by the femoral artery blood using a pump through bilateral common carotid arteries. EEG findings and qualitative CBF by 14C-iodoantipyrine autoradiography of this model were studied, which indicate the possible usefulness of this model in the basic investigation of cerebral ischemia.
A seven vessel occlusion model in the rat (occlusion of bilateral pterygopalatine, external carotid, common carotid arteries, and basilar artery) that produced complete forebrain ischemia without systemic hypotension was developted and used for following studies.
After 5min reperfusion following 30min ischemia, impaired reperfusion pattern was verified mainly in basal ganglia by CBF autoradiography, while, the recirculation pattern in mannitol pretreated animals was homogeneous and hyperemic. This indicates that mannitol prevented impairment of reperfusion after temporary ischemia.
Glucose and amino acid metabolism in reperfusion phase after ischemia was studied simultaneously by 18FDG and 14C-leucine multiple labeled autoradiography. The dissociation between blucose and amino acid metabolism was observed in deep part of the brain where the reperfusion tended to be impaired.
These results will provide us an important clue for undestanding pathophisiological corellation between metabolism and postischemic damage of the brain in reperfusion.
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