| Project/Area Number |
09670742
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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 | Iwate Medical University |
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Principal Investigator |
NAKAMURA Motoyuki Iwate Medical University Department of Medicine, Assistant Professor, 医学部, 講師 (40172449)
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| Co-Investigator(Kenkyū-buntansha) |
KAWAZOE Kohei Iwate Medical University Dept of Surgery, Professor, 医学部, 教授 (50075561)
SEGAWA Ikuo Iwate Medical University Dept of Medicine, Assistant Professor, 医学部, 講師 (50206611)
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| Project Period (FY) |
1997 – 1998
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| Project Status |
Completed (Fiscal Year 1998)
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| Budget Amount *help |
¥2,900,000 (Direct Cost: ¥2,900,000)
Fiscal Year 1998: ¥1,600,000 (Direct Cost: ¥1,600,000)
Fiscal Year 1997: ¥1,300,000 (Direct Cost: ¥1,300,000)
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| Keywords | Heart failure / Vessel / Endothelium / Nitric oxide |
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| Research Abstract |
Increased peripheral vascular tone is a critical factor in the deterioration of clinical stage and symptoms in chronic congestive heart failure (CHF) due to increased cardiac afterload and decreased nutritive skeletal muscle blood flow. We have found that endothelial function as represented by nitric oxide (NO) production shows significant attenuation with the progression of clinical severity of CHF as determined by New York Heart Association class (Ref 4 and 6). This endothelial dysfunction emerges in the early stages of CHF.In the advanced stage of the condition, both endothelium-dependent and endothelium-independent dilator mechanisms are impaired in limb resistance vessels. This occurs because vascular endothelial function, and especially NO production, is an important factor in the regulation of vasodilatory function as well as making an important contribution to vascular structure. Furthermore, although vasodilatory circulating factors such as natriuretic polypeptides and newly discovered adrenomedullin have been reported to be increased in heart failure, the vasodilatory potency of these polypeptide hormones in the limb vascular bed is significantly blunted (Ref. 5). These observations suggest that peripheral circulatory failure in CHF is due not only to simple arterial muscle constriction but also to structural and functional changes, including receptor and post-receptor levels in the vasculature. This vascular remodeling may be an important mechanism urderlying vasodilatory failure in both limb conduit and intra-skeletal muscle vessels, and may contribute significantly to left ventricular dysfunction and exercise intolerance in patients with heart failure (Ref 1).
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