| Project/Area Number |
03670683
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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 |
Cerebral neurosurgery
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| Research Institution | Osaka University |
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Principal Investigator |
YOSHIMINE Toshiki Osaka Univ., Med. School, Assistant, 医学部, 助手 (00201046)
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| Co-Investigator(Kenkyū-buntansha) |
KATO Amami Osaka Univ., Med. School, Assistant, 医学部, 助手 (00233776)
HAYAKAWA Toru Osaka Univ., Med. School, Professor, 医学部, 教授 (20135700)
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| Project Period (FY) |
1991 – 1992
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| Project Status |
Completed (Fiscal Year 1992)
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| Budget Amount *help |
¥2,100,000 (Direct Cost: ¥2,100,000)
Fiscal Year 1992: ¥900,000 (Direct Cost: ¥900,000)
Fiscal Year 1991: ¥1,200,000 (Direct Cost: ¥1,200,000)
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| Keywords | cerebral ischemia / microcirculation / superoxide / SOD / 赤血球 / 白血球 / 血小板 |
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| Research Abstract |
1. Pathologic process of microcirculatory disturbance in focal cerebral ischemia.
Our previous study demonstrated that the length of plasma-per fused microvessels decreased in the ischemic foci during the several hours of rat focal cerebral ischemia. The aim of the present investigation is to elucidate the mechanism of this microcirculatory disturbance.
2. Effect of superoxide dismutase (SOD).
When SOD was administered continuously during the several hours of acute focal cerebral ischemia, the microvascular patency was significantly preserved. Those data suggests that the formation superoxide during the acute stage of cerebral ischemia may cause endothelial injury and facilitate intravascular clot formation. The application of SOD also decreased the size of histologically noticeable damage.
3. Protection of ischemic brain damage via preservation of microcirculation.
The present study demonstrated SOD could be a useful agent to protect the brain against ischemia. Although SOD has been expected to reduce tissue damage directly by eliminating free radicals that cause tissue injury, the present study suggested preservation of microcirculation by SOD may also contribute to protect brain injury against cerebral ischemia. Since recombinant human SOD is available for clinical trial for cardiac attacks, the use of this agent against cerebral ischemia is also expected.
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