| Project/Area Number |
24590272
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Multi-year Fund |
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| Section | 一般 |
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| Research Field |
General physiology
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| Research Institution | Shinshu University |
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Principal Investigator |
KAWAI Yoshiko 信州大学, 学術研究院医学系, 准教授 (10362112)
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| Co-Investigator(Kenkyū-buntansha) |
OHHASHI Toshio 信州大学, 医学部, 特任教授 (80020832)
AJIMA Kumiko 信州大学, 学術研究院医学系, 助教 (70584051)
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| Project Period (FY) |
2012-04-01 – 2015-03-31
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| Project Status |
Completed (Fiscal Year 2014)
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| Budget Amount *help |
¥5,460,000 (Direct Cost: ¥4,200,000、Indirect Cost: ¥1,260,000)
Fiscal Year 2014: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2013: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2012: ¥2,990,000 (Direct Cost: ¥2,300,000、Indirect Cost: ¥690,000)
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| Keywords | 呼吸生理学 / 流れ刺激 / F1/FO ATP synthase / 炭酸ガス |
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| Outline of Final Research Achievements |
We studied physiological roles of flow through pulmonary arterioles in CO2 gas exchange. We established human pulmonary arteriolar endothelial cells (HPAoEC). Shear stress stimulation caused the co-release of H+ and ATP via the activation of F1/FO ATP synthase on the HPAoEC. Next, to further examine the validity of this concept in in vivo rabbit lungs, we investigated the effects of stenosis-induced changes in pulmonary blood flow on the end-expiratory CO2 gas pressure (PECO2), the maximal velocity of the pulmonary artery of anesthetized rabbits. In the experiment in which small pulmonary arteries were subjected to stenosis, the PECO2 fell rapidly. The flow-dependent changes in the PECO2 were reduced by the treatment with the F1/FO ATP synthase antibody. In conclusion, we have proposed a new concept of CO2 exchange, flow-mediated F1/FO ATP synthase-dependent H+ secretion, resulting in the facilitation of a dehydration reaction involving HCO3- in plasma and the excretion of CO2 gas.
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