| Project/Area Number |
01570293
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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 |
Hygiene
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| Research Institution | Miyazaki Medical College |
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Principal Investigator |
TAKENAKA Hitoshi Miyazaki Medical College, Faculty of Medicine ; Senior Research Associate., 医学部, 助手 (10179658)
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| Co-Investigator(Kenkyū-buntansha) |
HAMADA Minoru Miyazaki Medical College, Faculty of Medicine ; Professor., 医学部, 教授 (90039529)
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| Project Period (FY) |
1989 – 1991
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| Project Status |
Completed (Fiscal Year 1991)
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| Budget Amount *help |
¥1,000,000 (Direct Cost: ¥1,000,000)
Fiscal Year 1991: ¥500,000 (Direct Cost: ¥500,000)
Fiscal Year 1990: ¥500,000 (Direct Cost: ¥500,000)
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| Keywords | Ischemia / reperfusion / Peroxidation / Sarcoplasmic reticulum / Sarcolemma / Mitochondria / Cardiac performance / Heart transplantation / Univ. of Wisconssin in solution / 臓器浮腫 / 脂質過酸化 / ビタミンE / 心機能障害 / 虚血 / 再潅流 / 過酸化 / 酸素消費 / 細胞形質膜 / 活性酸素 / 過酸化脂質 / Ca能動輸送 / Ca-ATPase / 虚血障害 / 再灌流障害 / デフェロキサミン |
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| Research Abstract |
Cellular damages due to oxygen toxicity was analyzed by examining functions of sarcoplasmic reticulum(SR), sarcolemma(SL), and mitochondria(MIT). Cardiac performance after ischemia/reperfusion and pathological appearance after heterotopic transplantation of rat myocardium were also studied. Ischemia/reperfusion of rabbit hearts induced degradation of Ca pump protein, resulting ininhibition of Ca transport and Ca-dependent ATPase activities. SL functions were not inhibited by ischemia or reperfusion treatments. Reperfusion might also oxidize of the Ca pump protein. Rabbit skeletal SR was treated with a superoxide-generating system to mimic ischemia/reperfusion injury. Rapid oxidation of thiol residues inhibited ATPase and Ca transport activities, which were followed by a slow degradation of the pump protein and by slower lipid peroxidation. However, the mode of degradation of Ca pump in chemically oxidized skeletal SR was not necessarily similar to cardiac SR after ischemia/reperfusion.
… More
Cardiac performance of rat myocardium after hypothermic storage longer than 8 h showed energy dissipation between consumed oxygen and the total mechanical work, which was likely due to impaired mitochondria]respiration. Heterotopic transplantation of rat hearts after prolonged hypothermic storage revealed that reperfusion injury occurred in a early phase after starting reperfusion, was dependent on the storage conditions, and could be lowered by suppressing organ edema. The University of Wisconsin Cold Storage solution was effective to preserve heart from the above viewpoints. Administration of vitamin E prior to hepatic ischemia lowered mitochondria]damages.
In conclusion, reperfusion injury takes place in relatively early time of reperfusion and injury can be prevented by administration of a radical scavenger. It is also indicated that reperfusion injury occurs primarily in SR and MIT but not in SL and protein degradation is more serious than lipid peroxidation as etiology of ischemia/reperfusion injury. Less
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