| Project/Area Number |
05454270
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| Research Category |
Grant-in-Aid for General Scientific Research (B)
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| Allocation Type | Single-year Grants |
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| Research Field |
Circulatory organs internal medicine
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| Research Institution | Osaka University |
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Principal Investigator |
KUSUOKA Hideo Osaka Univ.Med.Sch.Associate Professor, 医学部, 助教授 (00112011)
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| Co-Investigator(Kenkyū-buntansha) |
UEHARA Toshiisa Osaka Univ.Hospital Lecturer, 医学部附属病院, 講師 (80243202)
NISHIMURA Tsunehiko Osaka Univ.Med.Sch.Professor, 医学部, 教授 (70237733)
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| Project Period (FY) |
1993 – 1995
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| Project Status |
Completed (Fiscal Year 1995)
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| Budget Amount *help |
¥6,300,000 (Direct Cost: ¥6,300,000)
Fiscal Year 1995: ¥2,100,000 (Direct Cost: ¥2,100,000)
Fiscal Year 1994: ¥1,900,000 (Direct Cost: ¥1,900,000)
Fiscal Year 1993: ¥2,300,000 (Direct Cost: ¥2,300,000)
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| Keywords | Myocardium / Glycolysis / Glucose uptake rate / Ischemia / Reperfusion / Magnetic resonance spectroscopy / 核磁気共鳴 / グルコース・トランスポータ / ATP(アデノシン3燐酸) / カルシウム・イオン / フェレット |
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| Research Abstract |
It has been reported in myocardium that energy for mechanical work is provided by oxidative phosphorylation whereas that to maintain ion homeostasis is generated by glycolysis. In this study, the effects of glycolytic inhibition on intramyocardial calcium homeostasis was investigated. Our results indicate that glycolytic ATP is not necessary to maintain calcium homeostasis in myocardium ; the sugar phosphates accumulated by glycolytic inhibition induce the calcium overload, but the further mechanism was not clarified. The glucose uptake in stunned myocardium was also investigated. The myocardium reperfused after a brief period of ischemia shows contractile dysfunction without necrosis, and is called as "stunned myocardium." Glycolysis and glycogenesis have been reported to be augmented in stunned myocardium, suggesting that the demand for exogenous glucose is increased in stunned myocardium. This study also seeks to quantify the increase in myocardial glucose uptake and to clarify the pathway of augmented glucose uptake in stunned myocardium. Glucose uptake rate was quantified from the time course of sugar phosphate resonance in rat myocardium using P-31 nuclear magnetic resonanceafter substitution of glucose by its analogue, 2-deoxyglucose. Our results indicate that the glucose uptake in stunned myocardium is augmented as high as in the myocardium stimulated by insulin, and that the augmented glucose uptake in stunned myocardium is maintained by glucose transporter. The increase of glucose uptake in reperfused myocardium was also confirmed clinically in patients with acute myocardial infarction using F-18 fluorodeoxyglucose and positron emmission tomography.
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