| Project/Area Number |
15590760
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Circulatory organs internal medicine
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| Research Institution | Kagoshima University |
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Principal Investigator |
OTSUJI Yutaka Kagoshima University, University Hospital, Faculty of Medicine and Dentistry, Assistant Professor, 医学部・歯学部附属病院, 講師 (30264427)
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| Co-Investigator(Kenkyū-buntansha) |
BIRO Sadatoshi Kagoshima University, University Hospital, Faculty of Medicine and Dentistry, Assistant Professor, 医学部・歯学部附属病院, 講師 (50244231)
TEI Chuwa Kagoshima University, Graduate School of Medical and Dental Sciences, Professor, 大学院・医歯学総合研究科, 教授 (10163891)
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| Project Period (FY) |
2003 – 2004
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| Project Status |
Completed (Fiscal Year 2004)
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| Budget Amount *help |
¥3,400,000 (Direct Cost: ¥3,400,000)
Fiscal Year 2004: ¥1,500,000 (Direct Cost: ¥1,500,000)
Fiscal Year 2003: ¥1,900,000 (Direct Cost: ¥1,900,000)
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| Keywords | ischemic mitral regurgitation / Renin angiotensin / remodeling / congestive heart failure / Ischemic mitral regurgitation / Ischemic / regurgitation / mitral |
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| Research Abstract |
Ischemic mitral regurgitation (MR) is an independent factor to worsen patients prognosis after the development of acute myocardial infarction. Outward displacement of papillary muscles due to left ventricular remodeling is the main cause of the ischemic MR. Renin-Angiotensin system (RAS) plays a central role in the genesis of left ventricular remodeling following myocardial infarction. Therefore, activation of RAS system may play an essential role in the genesis of ischemic MR, however, the role of RAS on the development of ischemic MR remains uninvestigated.
We hypothesized that development of ischemic MR can be attenuated by the absence of RAS activation due to gene abnormality. We produced acute myocardial infarction (AMI) with a similar size by ligation of left anterior descending artery in wild mouse as well as in Angiotensin II type 1A knocked out mouse. The LV dilatation was significantly greater in the wild compared to knocked out mouse. Ischemic MR was observed only in wild mouse (p<0.05). These suggest that RAS plays a central role in the genesis of ischemic MR after the development of AMI.
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