| Budget Amount *help |
¥5,330,000 (Direct Cost: ¥4,100,000、Indirect Cost: ¥1,230,000)
Fiscal Year 2013: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2012: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2011: ¥2,210,000 (Direct Cost: ¥1,700,000、Indirect Cost: ¥510,000)
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| Research Abstract |
After the onset of myocardial infarction, timely myocardial reperfusion is essential for myocardial salvage. However, reperfusion itself exacerbates injury of previously ischemic myocardium. (reperfusion injury). The excessive release of norepinephrine from cardiac sympathetic nerve terminal is known to be involved in the pathogenesis of ischemic cardiac injury. Prostanoids are bioactive lipid mediators consisting of prostaglandins (PGs) and thromboxane. In this research, we analyzed the mechanism of the cardioprotective action of prostanoids in myocardial infarction, using mice lacking the PGE2 receptors. In ischemic hearts, we demonstrated that endogenous PGE2 suppresses norepinephrine release via EP3 receptor.
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