| Project/Area Number |
23791681
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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 | Asahikawa Medical College |
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Principal Investigator |
TAMPO Akihito 旭川医科大学, 医学部, 助教 (80531524)
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| Project Period (FY) |
2011 – 2012
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| Project Status |
Completed (Fiscal Year 2013)
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| Budget Amount *help |
¥3,770,000 (Direct Cost: ¥2,900,000、Indirect Cost: ¥870,000)
Fiscal Year 2012: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2011: ¥2,600,000 (Direct Cost: ¥2,000,000、Indirect Cost: ¥600,000)
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| Keywords | 麻酔プレコンディショニング / ミトコンドリア / ナトリウムチャネル / 虚血再灌流傷害 / 虚血/再灌流傷害 / 周術期管理学 / イオンチャネル / マイトプラスト |
|---|
| Research Abstract |
We studied electrophysiological profiles of mitochondrial ion channels, which are known as important factors in anesthetic-induced preconditioning. Calcium overload is crucial mechanism to trigger cardiac ischemia/reperfusion injury. Ryanodine receptors play an important role as a mediator of calcium-induced calcium release in myocytes. We found several types of mitochondrial ion channels, and one of them may be mitochondrial ryanodine receptors. Cardiac sodium current was also recorded. APC resulted in the increase of the sodium current density. This change was correlated with the increase of the sodium channel expression. The steady-state inactivation curve was significantly shifted toward depolarizing direction, and recovery from inactivation was significantly accelerated. These electrophysiological changes by APC did not affect the action potential simulation.
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