| Project/Area Number |
12670036
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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 |
General physiology
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| Research Institution | Yamagata University |
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Principal Investigator |
TAKAHASHI Eiji Yamagata University School of Medicine, Physiology, Associate Professor, 医学部, 助教授 (30206792)
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| Project Period (FY) |
2000 – 2001
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| Project Status |
Completed (Fiscal Year 2001)
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| Budget Amount *help |
¥3,500,000 (Direct Cost: ¥3,500,000)
Fiscal Year 2001: ¥700,000 (Direct Cost: ¥700,000)
Fiscal Year 2000: ¥2,800,000 (Direct Cost: ¥2,800,000)
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| Keywords | heart / oxygen / mitochondrion / image processing / hypoxia / ischemia / cardiac hypertrophy / diffusion / ミオグロビン / 活性酸素 / 再灌流 |
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| Research Abstract |
Using a high-resolution spectrophotometric imaging system, relationship between intracellular oxygen supply and mitochondrial oxidative metabolism was examined in isolated single cardiomyocytes of the rat.
Specific questions were; whether intracellular diffusion of oxygen limits mitochondrial oxidative metabolism, 2. if so, how mitochondria deal with such heterogeneities of intracellular oxygen supply, and 3. what is the functional significance of cytosolic myoglobin. I found that cytosolic myoglobin certainly accelerates intracellular oxygen diffusion but diffusional oxygen supply may not always fully match the oxygen requirement of mitochondria particularly those located in the cell core. Thus, hypoxic core with metabolic inhibition (anoxic core) may be present in single cardiomyocytes with moderately elevated oxygen metabolism. I further demonstrated that this metabolic inhibition in the cell core is usually eliminated in mitochondria with intact respiratory control. Thus, in vivo cardiac myocytes can compensates for relatively slow intracellular oxygen diffusion.
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