| Project/Area Number |
13680816
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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 |
Nerve anatomy/Neuropathology
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| Research Institution | Tokyo Medical and Dental University |
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Principal Investigator |
KUROIWA Toshihiko Tokyo Med Dent Univ, Med Res Inst, Associate Professor, 難治疾患研究所, 助教授 (80129832)
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| Co-Investigator(Kenkyū-buntansha) |
YAMADA Ichiro TokyoMed Dent Univ School of Med, Associate Professor, 大学院・医歯学総合研究科, 助教授 (90182518)
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| Project Period (FY) |
2001 – 2002
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| Project Status |
Completed (Fiscal Year 2002)
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| Budget Amount *help |
¥3,300,000 (Direct Cost: ¥3,300,000)
Fiscal Year 2002: ¥1,100,000 (Direct Cost: ¥1,100,000)
Fiscal Year 2001: ¥2,200,000 (Direct Cost: ¥2,200,000)
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| Keywords | Cerebral ischemia / recirculation / Mongolian gerbil / C57BI / 6J mouse / neuronal death / Cerebral infarction / MRI / C57Bl / 一過性脳虚血 / 神経脱落症状 / スナネズミ / 拡散係数 / 超微細構造 |
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| Research Abstract |
We studied pathophysiological and neurological changes after transient cerebral ischemia induced by by clot embolization and thrombolysis in C57B1/6J mice, and compared the results with a cerebral ischemia induced by temporary ligation of the common carotid artery. Clot embolization and thrombolysis induced a transient CBF decrease for approximately 30 min. Neurological symptoms including spontaneous locomotion and failed grid catching rate was monitored during the observation period of 24 h postischemia. Common carotid artery was temporary ligated to induce cerebral ischemial in gerbil. In mice, frozen brains were processed for mapping of tissue ATP content, Cerebral Protein Synthesis (CPS) and TUNEL staining positive area. In gerbil, we monitored neurological dysfunction for 4 weeks after transient ischemia, and the results were correlated with the histological changes and MRI findings. After clot embolizatin, rCBF reduced to 19.8 +/- 11% of the control level and gradually recovered thereafter. Neurological deficit score gradually became worse during postischemia. The area of CPS reduction was 28.7 +/-11.5% and 38.5 +/- 20.6% of the control at 6 h and 24 h postischemia, respectively. ATP content also reduced to 8.7 +/- 5.4% and 38.4 +/- 22% of the control at 6h and 24h postishemia, respectively. Area of TUNEL positive cells is strikingly similar to the area of CPS reduction at 24 h postischemia. Comparison of the psotischemic changes of neurological and pathophysiological parameters indicate that clot embolization model of cerebral ischemia evolves pathophysiological changes similar to human embolic ischemia and therefore suitable model of experimental cerebral ischemia.
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