Project/Area Number |
01570870
|
Research Category |
Grant-in-Aid for General Scientific Research (C)
|
Allocation Type | Single-year Grants |
Research Field |
麻酔学
|
Research Institution | University of the Ryukyus, Faculty of Medicine |
Principal Investigator |
YUSA Toshiko Faculty of Medicine, Anesthesiology, Associate professor, 医学部, 助教授 (30032329)
|
Co-Investigator(Kenkyū-buntansha) |
MIYAMOTO Koho Faculty of Medicine, Physiology, Associate Professor, 医学部, 助教授 (20014350)
TAKARA Eiichi Faculty of Medicine, Neurosurgery, Associate Professor, 医学部, 助教授 (30075709)
|
Project Period (FY) |
1989 – 1991
|
Project Status |
Completed (Fiscal Year 1991)
|
Budget Amount *help |
¥2,200,000 (Direct Cost: ¥2,200,000)
Fiscal Year 1991: ¥600,000 (Direct Cost: ¥600,000)
Fiscal Year 1990: ¥600,000 (Direct Cost: ¥600,000)
Fiscal Year 1989: ¥1,000,000 (Direct Cost: ¥1,000,000)
|
Keywords | brain ischemia / brain ischemia-reperfusion / oxygen free radical / brain anoxia / monoamine neurotransmitter / 虚血ー再潅流 / 脳血流量 / 脳組織血流量 / 脳モノアミン神経伝達物質 / ホモバニリン酸 / 5-ヒドロキシインド-ル酢酸 |
Research Abstract |
1) Histologic changes after transient brain ischemia by air embolism (using air embolism models in rats compressed to 6 ATA): After rapid decompression from 6 ATA air, the blood-brain barrier and cerebral microcirculation are immediately derranged by intra-vasculary formed air bubbles. Light microscopic examination demonstrated the edematous brain tissue with enlarged perivascular space and degenerative nerve cells. 2) Origin of oxygen free radical generation in anoxic cat brain: The effect of anoxia on the levels of monoamine neurotransmitters and their metabolites in the brain ECF was studied in cats using brain microdialysis combined with HPLC. Anoxia caused an immediate linear decrease of monoamine metabolites (5- HIAA and HVA) and an abrupt increase of monoamines (5-HT, NA or DA). These results , taken together with the existence of an electrically coupled system for the transport of HVA and 5-HIAA to brain ECF, suggest that increased monoamines (especially NA and DA) during anoxia
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or ischemia possibly generate oxygen free radicals during reoxygenation or reperfusion. 3) Effect of ischemia-reperfusion on superoxide generation in rat brain in vivo, in situ: Using cypridina luciferin analogus (CLA,MCLA) as sensitive and specific chemiluminescence probes for superoxide and a sensitive phooton counter, superoxide generation in vivo, in situ was investigated in rats subjected to incomplete or complete brain ischemia followed by reperfusion. As a result, increased superoxide generation was not detected within 2 hours after reperfusion. 4) Oxygen free radical generation in vivo, in situ by ischemia-reperfusion: Using brain in vivo microdialysis system and detecting hydrogen peroxide as a maker of oxygen free radical, hydrogen peroxide in perfusate from the brain cortex was measured by a HPLC/isoluminol chemiluminescence assay in rats subjected to 15 or 30 min complete ischemia followed by reperfusion. As results, 30-90 min after reperfusion, increased hydrogen peroxide generation was detected in rats subjected to 30 min ischemia. Less
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