| Project/Area Number |
23591046
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Multi-year Fund |
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| Section | 一般 |
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| Research Field |
Circulatory organs internal medicine
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| Research Institution | The University of Tokushima |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
SATA Masataka 徳島大学, ヘルスバイオサイエンス研究部, 教授 (80345214)
HARADA Masafumi 徳島大学, ヘルスバイオサイエンス研究部, 教授 (20228654)
AIHARA Kenichi 徳島大学, ヘルスバイオサイエンス研究部, 講師 (70372711)
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| Project Period (FY) |
2011 – 2013
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| Project Status |
Completed (Fiscal Year 2013)
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| Budget Amount *help |
¥4,940,000 (Direct Cost: ¥3,800,000、Indirect Cost: ¥1,140,000)
Fiscal Year 2013: ¥910,000 (Direct Cost: ¥700,000、Indirect Cost: ¥210,000)
Fiscal Year 2012: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
Fiscal Year 2011: ¥2,210,000 (Direct Cost: ¥1,700,000、Indirect Cost: ¥510,000)
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| Keywords | 心筋梗塞後心筋リモデリング / 心臓リモデリング / ヘパリンコファクターII / 急性心筋梗塞 |
|---|
| Research Abstract |
Reperfusion therapy has been shown to reduce the acute phase mortality of patients with acute myocardial infarction (AMI). However, cardiac remodeling in chronic phase reduces cardiac function and results in heart failure. Heparin cofactor II(HCII), a serin peotease inhibitor, exerts pleiotropic effects through inactivation of thrombin action in various tissue. We examined the effects of HCII against cardiac remodeling in patients with AMI. Left ventricular end-diastolic volume significantly decreased at chronic phase in patients with high plasma HCII activity, suggesting anti-remodeling effects of HCII.
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