Coronary Circulation in the Failing Heart

Research Project

Project/Area Number	08670813
Research Category	Grant-in-Aid for Scientific Research (C)
Allocation Type	Single-year Grants
Section	一般
Research Field	Circulatory organs internal medicine
Research Institution	Fukushima 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)
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.