| Project/Area Number |
08457350
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| Research Category |
Grant-in-Aid for Scientific Research (B)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Thoracic surgery
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| Research Institution | Osaka University |
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Principal Investigator |
TAKAHASHI Toshiki Osaka University Medical School, Assistant Professor, 医学部, 助手 (50263257)
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| Co-Investigator(Kenkyū-buntansha) |
ICHIKAWA Hajime Osaka University Medical School, Assistant Professor, 医学部, 助手
MASAI Takahumi Osaka University Medical School, Assistant Professor, 医学部, 助手 (30273650)
IMAGAWA Hiromu Osaka University Medical School, Assistant Professor, 医学部, 助手 (90273622)
SAWA Yoshiki Osaka University Medical School, Assistant Professor, 医学部, 助手 (00243220)
竹谷 哲 大阪大学, 医学部・附属病院, 医員
鍵崎 康治 大阪大学, 医学部・附属病院, 医員
西村 元延 大阪大学, 医学部, 助手 (90291442)
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| Project Period (FY) |
1996 – 1997
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| Project Status |
Completed (Fiscal Year 1997)
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| Budget Amount *help |
¥6,300,000 (Direct Cost: ¥6,300,000)
Fiscal Year 1997: ¥2,400,000 (Direct Cost: ¥2,400,000)
Fiscal Year 1996: ¥3,900,000 (Direct Cost: ¥3,900,000)
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| Keywords | Cardiac Hypertrophy / Heart Failure / Gene expression |
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| Research Abstract |
Myocardial hypertrophy is a basic adaptive mechanism of the heart to compensate for an increased mechanical load. Heart failure is final presentation of cardiovascular disease, such as coronary artery disease, hypertension, valvular heart disease, myocarditis and others. The pathogenetic mechanisms responsible for the transition to cardiac dysfunction and heart failure are not well understood. Volume-overloaded rat hearts were established by A-V shunt between abdominal aorta and inferior caval vein. Immunohistochemical investigations of proto-oncogene proteins were performed in the presence. The myocytes of volume-overloaded hearts were significantly larger in diameter than control hearts on 14th day after A=V shunt. The weight of volume-overloaded hearts was also significantly larger than control hearts. In nuclei of myocytes of volume-overloaded hearts, the maximum expression of Fos and Myc protein was observed on the 2nd day after A-V shunt. After the 2nd day, the expression decreased gradually. In the human heart, however, it has not been clarified whether these proto-oncogenes are related to contractile impairment and structural alteration of the myocardium. The present study is designed to investigate the relationship between the C-Myc protein expression in the myocardium and the myocardial contractile dysfunction in patients with chronic aortic regurgitation. C-Myc was detected in nine of 12 present patients but in none of the normal controls. The degree of C-Myc expression had significant positive correlations with EF and ESS/ESVI and significant negative correlations with ESVI,CD and FC,which suggested that the degree of C-Myc expression may have a significant negative correlation with myocardial contractility and myocardial hypertrophy. Conclusion : C-Myc expression may be related to the pathogenesis of myocardial remodeling in patients with chronic aortic regurgitation.
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