| Project/Area Number |
15591478
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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 |
Thoracic surgery
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| Research Institution | KYUSHU UNIVERSITY |
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Principal Investigator |
TOKUNAGA Shigehiko Kyushu University, Department of cardiovascular surgery, facility of Medicine, Research Associate, 病院, 助手 (80346775)
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| Co-Investigator(Kenkyū-buntansha) |
NISHIDA Takahiro Kyushu University, Department of cardiovascular surgery, facility of Medicine, Research Associate, 病院・助手 (50284500)
MORITA Shigeki Kyushu University, Graduate school of Medicine, Associate Professor, 大学院・医学研究院, 助教授 (70243938)
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| Project Period (FY) |
2003 – 2004
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| Project Status |
Completed (Fiscal Year 2004)
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| Budget Amount *help |
¥2,700,000 (Direct Cost: ¥2,700,000)
Fiscal Year 2004: ¥1,400,000 (Direct Cost: ¥1,400,000)
Fiscal Year 2003: ¥1,300,000 (Direct Cost: ¥1,300,000)
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| Keywords | Free radical / reperfusion injury / electron paramagnetic resonance / Neutrophil |
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| Research Abstract |
Previous studies have suggested that the depletion of leukocytes during reperfusion decreases activation of inflammatory cytokines or the no-reflow phenomenon. On the other hand, few studies mention leukocyte-derived free radical-mediated reperfusion injury. This study attempts to clarify the effect of leukocyte-derived free radicals in reperfusion injury by measuring the total amount of hydroxyl radicals using electron paramagnetic resonance. Twelve rabbits were divided into two groups, a leukocyte depletion filter(IDF) and control group. Isolated rabbit hearts of both groups were subjected to 30 minutes of normothermic global ischemia then reperfused with support rabbit blood. Myocardial samples were taken and reacted with hydroxyl TEMPO (0.1 mmol/L), a hydroxyl radical-specific spine probe. The decay rate of the electron spin resonance signal, which directly reflects hydroxyl radical production, was measured. Cardiac function was measured until sixty minutes after reperfusion. Levels of nitric oxide, an important free radical scavenger, were also measured to investigate their free radical scavenging ability and effect on cardiac function. The signal decay rates of the LDF and control groups were 0.98±0.30 and 2.06±0.78×10^<-2>/min, respectively, two minutes after reperfusion. Hearts treated with a leukocyte depletion filter showed better functional recovery and lower creatine kinase MB leakage. Nitric oxide concentrations were higher in the LDF group than the control group at 2 and 15 minutes after reperfusion. Leukocyte depletion during reperfusion decreased the production of hydroxyl radicals and suppressed nitric oxide consumption thereby attenuating reperfusion injury in the cross-circulation rabbit heart model.
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