| Project/Area Number |
13671561
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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 |
Anesthesiology/Resuscitation studies
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| Research Institution | TOHOKU UNIVERSITY |
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Principal Investigator |
HORINOUCHI Takashi Tohoku University, Graduate School of Medicine, Associate Professor, 大学院・医学系研究科, 助教授 (00229238)
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| Co-Investigator(Kenkyū-buntansha) |
SATOH Minato Tohoku University, University Hospital, Research Associate, 医学部附属病院, 助手 (80333798)
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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 |
¥3,700,000 (Direct Cost: ¥3,700,000)
Fiscal Year 2002: ¥500,000 (Direct Cost: ¥500,000)
Fiscal Year 2001: ¥3,200,000 (Direct Cost: ¥3,200,000)
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| Keywords | Transient Spinal Cord Ischemia / Hyperbaric Oxygenation / nNOS / 3-Nitrotyrosine / GDNF / Apoptosis / 遅発性神経細胞死 / 神経栄養因子 |
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| Research Abstract |
The reproducible spinal cord ischemic models in rabbits were made with infalation of a pulmonary catheter in abdominal aorta for 15MIN. After ischemic insult rabbits were assigned into two groups (Hyperbaric oxygenation treatment group or control group). Hyperbaric oxygenation was performed for 1 hr at 3 atm absolute with 100% oxygen at 30 MIN after reperfusion. All rabbits were euthanaized and spinal cords were picked up quickly for further investigation.
In control group each rabbit showed progressive paraplegia and decrease in the number of motor neurons was observed histologically. These Apoptotic involvements were confirmed by the induction of Caspase-3 like activity at 24 hr after ischemic insult immunohistologically. At 8 hr after reperfusion expression of nNOS followed by excitation of NMDA receptor and induction of 3-nitrotyrosine were observed therefore we concluded this signaling is crucial pathway for neuronal death.
In hyperbaric oxygenation group each rabbit showed histological and neurological improvement and expression of nNOS and induction of 3-nitrotyrosine were rarely observed therefore we concluded the effect of hyperbaric oxygenation is exerted by inhibiton of this signaling.
We further investigated the induction of GDNF, neurotrophic factor, as a neuro-survival signaling, but there is no prominent difference in intensity and way of induction between two groups, therefore we concluded the inhibitory effect against nNOS and 3-nitortyrosine with hyperbaric oxygenation has nothing to do with the induction of GDNF.
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