The effect of ischemia and reperfusion injury on the endothelial cells
Project/Area Number |
25462819
|
Research Category |
Grant-in-Aid for Scientific Research (C)
|
Allocation Type | Multi-year Fund |
Section | 一般 |
Research Field |
Emergency medicine
|
Research Institution | Hamamatsu University School of Medicine |
Principal Investigator |
Obata Yukako 浜松医科大学, 医学部附属病院, 助教 (90432210)
|
Project Period (FY) |
2013-04-01 – 2017-03-31
|
Project Status |
Completed (Fiscal Year 2016)
|
Budget Amount *help |
¥4,550,000 (Direct Cost: ¥3,500,000、Indirect Cost: ¥1,050,000)
Fiscal Year 2015: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2014: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2013: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
|
Keywords | 虚血再灌流 / 低酸素 / 血管内皮 / エネルギー枯渇 |
Outline of Final Research Achievements |
Endothelial cells play important roles such as organs during inflammation and ischemia and reperfusion injury and it has been known that they work as mediator. We measured the intracellular Ca2+ concentration of porcine aortic endothelial cells as endothelial function, when the energy depletion by chemical agents and the energy supply with medium was caused on the cells. We found that the bradykinin-induced Ca2+ response and the thapsigargin-induced Ca2+ response partly suppressed after the energy depletion with KCN and 2-Deoxy-D-glucose and the energy supply with medium. These findings suggest that endothelial function was altered, at least in part, by the energy depletion and that the change of endothelial function occurs in the clinical hypoxia and reperfusion.
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Report
(5 results)
Research Products
(1 results)