| Project/Area Number |
08670813
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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 | Fukushima Medical College |
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Principal Investigator |
SAITO Tomiyoshi Fukushima Medical College First Dept.of Int.Med., Associate Prof., 医学部, 助手 (30235056)
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| Co-Investigator(Kenkyū-buntansha) |
SAITO Shu-ichi Fukushima Medical College First Dept.of Int.Med., Associate Prof., 医学部, 助手 (20274962)
MARUYAMA Yukio Fukushima Medical College First Dept.of Int.Med., Prof., 医学部, 教授 (90004712)
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| Project Period (FY) |
1996 – 1997
|
| Project Status |
Completed (Fiscal Year 1997)
|
| Budget Amount *help |
¥2,300,000 (Direct Cost: ¥2,300,000)
Fiscal Year 1997: ¥1,000,000 (Direct Cost: ¥1,000,000)
Fiscal Year 1996: ¥1,300,000 (Direct Cost: ¥1,300,000)
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| Keywords | Heart Failure / Coronary Circulation / Nitric Oxide / Sympathetic Nerve / α受容体 / Nitric oxide / アデノシン / アセチルコリン |
|---|
| Research Abstract |
To clarify the roles of endothelium-dependent and independent and adrenergic regulations on coronary circulation in heart failure, coronary diastolic pressure-flow (P-F) relationships were analyzed. Flow probe was placed around the coronary artery, and complete atrioventricular block was produced. Three weeks after pacing at 240/min, right atrial and left ventricular end-diastolic pressures increased. Plasma norepinephrine increased. The slope of P-F relationship steepened with slight increases in the zero-flow pressure (Pf=0) after pacing. After L-NAME,Pf=0 increased equally before and after pacing, and the slope after pacing declined more than that before pacing. Acetylcholine-induced coronary vasodilation was not altered, but adenosine-induced vasodilation was attenuated after pacing. Exogenously administrerd norepinephrine caused tendency of vasoconstriction before pacing, but slight vasodilation after pacing. Alpha 2 adnenocepor-mediated vasodilation mainly contributed to it. These results suggest that impairment of endothelium-independent vasodilation contributes to progression of heart failure, and additional sympathetic stimulation leads to a cantributory factor for the enhancement of coronary blood flow in heart failure.
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