| Project/Area Number |
21790755
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Single-year Grants |
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| Research Field |
Circulatory organs internal medicine
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| Research Institution | University of Occupational and Environmental Health, Japan |
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Principal Investigator |
NAKATA Sei University of Occupational and Environmental Health, Japan, 医学部, 非常勤医師 (20535223)
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| Project Period (FY) |
2009 – 2010
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| Project Status |
Completed (Fiscal Year 2010)
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| Budget Amount *help |
¥4,160,000 (Direct Cost: ¥3,200,000、Indirect Cost: ¥960,000)
Fiscal Year 2010: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
Fiscal Year 2009: ¥2,210,000 (Direct Cost: ¥1,700,000、Indirect Cost: ¥510,000)
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| Keywords | 分子血管病態学 / 一酸化窒素合成酵素 / アンジオテンシンII / 心不全 / 心肥大 / 動脈硬化 / 高脂血症 / LDL受容体 |
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| Research Abstract |
A spontaneous myocardial infarction based on metabolic syndrome and coronary arteriosclerosis was observed in the triply NOS(-/-) mice that we have recently developed. Then, I hit on an idea using this mouse to research for the novel therapy of a myocardial infarction. Long-term treatment with olmesartan (angiotensin II type 1 receptor blocker) significantly improved all these metabolic phenotypes and coronary lesion formation in the triply NOS(-/-) mice. Long-term treatment with atorvastatin (HMG-CoA reductase inhibitor) also significantly alleviated all the metabolic phenotypes and coronary lesion formation in the triply NOS(-/-) mice. Furthermore, long-term treatment with isosorbide dinitrate (NO donor) significantly ameliorated all the metabolic phenotypes in the triply NOS(-/-) mice. These results indicate beneficial effect of these medicines for the metabolic syndrome and coronary lesion formation, which are causes of myocardial infarction, demonstrating important findings in therapeutic for myocardial infarction. The prevent effect for myocardial infarction by these medicines is expected, and is presently under study.
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