| Project/Area Number |
16590107
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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 |
Medical pharmacy
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| Research Institution | Niigata University |
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Principal Investigator |
TAKAHASHI Toshihiro Niigata University, Institute of Medicine and Dentistry, Professor, 医歯学系, 教授 (70143039)
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| Co-Investigator(Kenkyū-buntansha) |
WATANABE Ken-ichi Niigata University of Pharmacy and Applied Life Sciences, Department of Clinical Pharmacology, Professor, 臨床薬理学教室, 教授 (70175090)
NAITOH Makoto Niigata University, Institute of Medicine and Dentistry, Professor, 医歯学系, 教授 (30045786)
IZUMIKAWA Takuji Niigata University, Radioisotope Center, Associate Professor, アイソトープ総合センター, 助教授 (60282985)
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| Project Period (FY) |
2004 – 2005
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| Project Status |
Completed (Fiscal Year 2005)
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| Budget Amount *help |
¥3,000,000 (Direct Cost: ¥3,000,000)
Fiscal Year 2005: ¥1,000,000 (Direct Cost: ¥1,000,000)
Fiscal Year 2004: ¥2,000,000 (Direct Cost: ¥2,000,000)
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| Keywords | heart function / heart accumulating radiopharmaceutical / labeled fatty acid / myocardial fatty acid metabolism / labeled sugar / labeled agent for sympathetic nervous function / myocardial energy efficiency / 心筋機能評価 / エネルギー獲得系 / 分離測定 |
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| Research Abstract |
In this study, we propose the evaluational method of two kinds of heart functions using dual heart accumulating radiopharmaceuticals. The used radiopharmaceuticals were [I-125]9MPA for myocardial fatty acid metabolism, [I-125]MIBG for study of heart sympathetic nervous function and [C-14]2DG for sugar metabolism and the used animals were normal rat (standard heart) and CHF (chronic heart failure) rat, which is a rat model of dilated cardiomyopathy induced by autoimmune myocarditis. Using above-mentioned materials, we performed some animal studies about time (after injection)-heart uptake study, fatty acid metabolic study, autoradiography, etc. In result, in the CHF heart, both the fatty acid metabolic function and the heart sympathetic nervous function were damaged, but the sugar metabolic function was activated. These results have been suggested that the energy efficiency in the CHF heart changes from fatty acid use to sugar use. Further, it has been also shown that the heart size becomes larger with increasing the severity of heart damage (the relatively good correlation between heart weight (heart size) and 9MPA/MIBG heart uptake) and in the CHF heart, the storage metabolic route is mainly damaged by the fatty acid metabolic study.
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