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Coronary Circulation in the Failing Heart

Research Project

Project/Area Number 08670813
Research Category

Grant-in-Aid for Scientific Research (C)

Allocation TypeSingle-year Grants
Section一般
Research Field Circulatory organs internal medicine
Research InstitutionFukushima Medical College

Principal Investigator

SAITO Tomiyoshi  Fukushima Medical College First Dept.of Int.Med., Associate Prof., 医学部, 助手 (30235056)

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)
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)
KeywordsHeart 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.

Report

(3 results)
  • 1997 Annual Research Report   Final Research Report Summary
  • 1996 Annual Research Report
  • Research Products

    (2 results)

All Other

All Publications (2 results)

  • [Publications] T.Saito, et al.: "NO-mediated increase in diastolic coronary flow is not neecssarily impaired in heart failure." Circulation. 94(8). I-495 (1996)

    • Description
      「研究成果報告書概要(和文)」より
    • Related Report
      1997 Final Research Report Summary
  • [Publications] Tomiyoshi saito, et al.: "NO-mediated increase in diastolic coronary flow is not necessarily impaired in heart failure." Circulation. 94(8). I-495 (1996)

    • Description
      「研究成果報告書概要(欧文)」より
    • Related Report
      1997 Final Research Report Summary

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Published: 1996-04-01   Modified: 2016-04-21  

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