| Project/Area Number |
01570485
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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 |
Circulatory organs internal medicine
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| Research Institution | Osaka University |
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Principal Investigator |
MATSUMOTO Masayasu Osaka University, Medical School, Assistant Prof., 医学部, 助手 (20192346)
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| Co-Investigator(Kenkyū-buntansha) |
FUKUNAGA Ryuzo Osaka University, Medical School, Assistant Prof,, 医学部, 助手 (50218947)
北川 一夫 大阪大学, 医学部附属病院, 医員
半田 伸夫 大阪大学, 医学部附属病院, 医員
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| Project Period (FY) |
1989 – 1990
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| Project Status |
Completed (Fiscal Year 1990)
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| Budget Amount *help |
¥2,100,000 (Direct Cost: ¥2,100,000)
Fiscal Year 1990: ¥1,000,000 (Direct Cost: ¥1,000,000)
Fiscal Year 1989: ¥1,100,000 (Direct Cost: ¥1,100,000)
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| Keywords | Mongolian Gerbil / Cerebrag Ischemia / Selective Vulnerability / Free Radical / Microcirculation / Delayed Neuronal Death / Immundhistochemistry / Blood-brain Barrier / 微小循環 / 血液・脳関門 / 微小管結合蛋白2 / シナプシンI |
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| Research Abstract |
In the present study, we attempted to investigate the pathophysiological roles of microcirculatory derangement in the neuronal selective vulnerability to cerebral ischemia by using stroke-prone gerbils, which should develop typical stroke symptoms after unilateral common carotid occlusion and through research works from 1989 to 1990, we could obtain the following results : 1. Postsynaptic sides of the neurons, visualized by immunostaining for microtubule-associated protein 2, were more vulnerable to ischemic damage than presynaptic sides of the neurons, visualized by immunostaining for synapsin I. 2. The anatomical sites where the immunohistochemical lesions develop early were often the "blood flow cliff" areas, where the area with extremely low cerebral blood flow (CBF) and that with substantial residual CBF merged together. 3. Pre-ischemic treatment by pyran conjugated superoxide dismutase showed clear protective effects against both the neuronal damages detected after 5 min ischemia
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and the delayed neuronal death, though no clear beneficial effects by post-ischemic treatment by this drug, suggesting free radical generation at the "blood flow cliff" areas during brief period when ischemia plays a pivotal role in triggering the ischemic neuronal damages causing delayed neuronal death at the selectively vulnerable areas of the brain. 4. In a newly established reproducible gerbil model of ischemia-reperfusion vasogenic brain edema, we could clarify the lateral part of the thalamus was more susceptible to blood-brain barrier damage than any other region of the brain and the massive albumin extravasation seen in the thalamus early in the reperfusion period might be partly caused by the continuous influx of serum albumin from the vulnerable lateral part of the thalamus. These results clearly demonstrated that microcirculatory derangements during and after cerebral ischemia play a quite important pathological roles in determining the selective vulnerability of the neurons to ischemic insult. Less
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