© 1996 American Heart Association, Inc.
Articles |
Role of Endothelium-Derived Nitric Oxide in Coronary Vasodilatation Induced by Pacing Tachycardia in Humans
the Research Institute of Angiocardiology and the Cardiovascular Clinic, Faculty of Medicine, Kyushu University, Fukuoka, Japan.
Correspondence to Kensuke Egashira, MD, Research Institute of Angiocardiology and Cardiovascular Clinic, Kyushu University School of Medicine, 3-1-1 Maidashi, Higashi-ku, Fukuoka 812-82, Japan.
Endothelium-derived NO contributes to the control of coronary perfusion. We investigated the roles of NO in the metabolic coronary vasodilatation induced by rapid pacing in humans. We evaluated the dilatation of large epicardial and resistance coronary arteries during rapid atrial pacing before and after intracoronary infusion of NG-monomethyl-L-arginine (L-NMMA), an inhibitor of NO synthesis, in 19 patients without significant coronary artery disease. The diameter of the large epicardial coronary artery and coronary blood flow (CBF) were assessed by quantitative coronary arteriography and by a Doppler flow velocity measurement. An increase in the heart rate increased CBF (P<.01) and the coronary artery diameter (P<.05). L-NMMA at a total dose of 200 µmol reduced basal CBF but did not significantly affect basal coronary artery diameter, arterial pressure, or heart rate. L-NMMA inhibited the pacing-induced dilatation of the large coronary arteries (P<.05) but did not affect pacing-induced increases in CBF. L-NMMA inhibited the acetylcholine-induced increase in CBF (P<.01) and acetylcholine-induced dilatation of the large epicardial coronary artery (P<.05). These results show that the contribution of NO to the metabolic vasodilatation during rapid pacing may differ between large epicardial and resistance coronary arteries in patients without significant coronary artery disease.
Key Words: nitric oxide • coronary circulation • endothelium-derived relaxing factor • acetylcholine
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