| Project/Area Number |
11470271
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| Research Category |
Grant-in-Aid for Scientific Research (B).
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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 | KYOTO UNIVERSITY |
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Principal Investigator |
HIRATA Toshiki Kyoto University, Faculty of Medicine, Assistant Professor, 医学研究科, 助手 (70281110)
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| Co-Investigator(Kenkyū-buntansha) |
WADA Hiromi Kyoto University, Faculty of Medicine, Professor, 医学研究科, 教授 (90167205)
FUKUSE Tatsuo Kyoto University, Faculty of Medicine, Assistant Professor, 医学研究科, 助手 (90263152)
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| Project Period (FY) |
1999 – 2000
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| Project Status |
Completed (Fiscal Year 2000)
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| Budget Amount *help |
¥5,200,000 (Direct Cost: ¥5,200,000)
Fiscal Year 2000: ¥2,900,000 (Direct Cost: ¥2,900,000)
Fiscal Year 1999: ¥2,300,000 (Direct Cost: ¥2,300,000)
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| Keywords | Lung transplantation / non-heart-beating donor / ischemic tolerance / mitochondria / preconditioning / ischemia-reperfusion injury / preconditoning |
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| Research Abstract |
Lung transplantation has become one of the main therapeutic modalities for end-stage lung diseases, but lack of donors has been the major problem. One possibility of efforts to obtain organs from other sources of is transplantation of lungs donated from cadavers after cardiac arrest. However, short time limit is the major problem in the clinical application of lungs of cardiac arrested donors.
In study 1, we evaluated the role of energy state in primary graft dysfunction which is crucial in lung transplantation. It was found that reperfusion lung injury following cold preservation was closely correlated with decreased levels of intrapulmonary high-energy phosphate compounds after reperfusion and that the addition of ATP and MgCl2 to the preservation solution attenuated reperfusion injury following cold ischemia in rat lungs. In study 2, we evaluated the possibility of using pulmonary mitochondrial respiratory functions as early markers of ischemic lung viability in non-heart-beating donors. It was found that the mitochondrial respiratory control ratio may be a useful early marker for lung viability after cardiac arrest. In study 3, we investigated whether or not chemical preconditioning can suppress ischemia-reperfusion injury in cardiac-arrested lungs. We found that chemical preconditioning reduced ischemia-reperfusion injury in cardiac arrested rat lungs. These results may lead to achieve a realistic alternative to expand the donor pool for lung transplantation.
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