| Project/Area Number |
24791590
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Multi-year Fund |
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| Research Field |
Anesthesiology/Resuscitation studies
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| Research Institution | Shiga University of Medical Science |
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Principal Investigator |
KOJIMA Akiko 滋賀医科大学, 医学部, 助教 (50447877)
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| Research Collaborator |
MATSUURA Hiroshi 滋賀医科大学, 医学部, 教授 (60238962)
OMATSU Mariko 滋賀医科大学, 医学部, 准教授 (80161397)
KITAGAWA Hirotoshi 滋賀医科大学, 医学部, 教授 (50252391)
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| Project Period (FY) |
2012-04-01 – 2014-03-31
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| Project Status |
Completed (Fiscal Year 2013)
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| Budget Amount *help |
¥4,160,000 (Direct Cost: ¥3,200,000、Indirect Cost: ¥960,000)
Fiscal Year 2013: ¥2,470,000 (Direct Cost: ¥1,900,000、Indirect Cost: ¥570,000)
Fiscal Year 2012: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
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| Keywords | 麻酔学 / 心筋虚血再灌流傷害 / 心筋保護 / 吸入麻酔薬 / Ca2+輸送タンパク質 / Ca2+イメージング法 / パッチクランプ法 / 虚血再灌流傷害 |
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| Research Abstract |
The disturbance of intracellular Ca2+ homeostasis occurs in myocaridium during ischemia/reperfusion and is responsible for cellular injury leading to cardiac dysfunction, namely ischemia/reperfusion injury. We investigated the molecular mechanisms underlying cardioprotective action of the volatile anesthetic sevoflurane on ischemia/reperfusion injury, using experimental models for Ca2+ overload-induced cellular injuries mediated by oxidative stress or store operated Ca2+ entry (SOCE) process.
We found that sevoflurane protects mouse ventricular myocytes against these cellular injuries, presumably by affecting multiple Ca2+ transporting pathway, including ryanodine receptor, Na+/Ca2+ exchanger and SOCE channel. These actions appear to produce the cardioprotection on ischemia/reperfusion injury associated with intracellular Ca2+ overload.
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