Endothelium determines flow-dependent dilation of the epicardial coronary artery in dogs

Abstract

The mechanisms of epicardial coronary artery dilation alter reactive hyperemia were studied in instrumented conscious dogs. A pair of ultrasonic crystals, an electromagnetic flow probe and a cuff occluder were placed on the left circumflex coronary artery in 12 mongrel dogs under sterile conditions. Reactive hyperemia after 20 s of coronary occlusion dilated the epicardial coronary artery by 120 ± 14 μm (3.8 ± 0.6%, p < 0.01) from 3.167 ± 0.345 mm. This reactive dilation was abolished by flow-limiting coronary stenosis. However, vasodilation after nitroglycerin was 168 ± 26 μm (5.1 ± 0.5%) and 162 ± 27 μm (4.9 ± 0.6%), respectively, before and after flow limitation.After removal of the endothelium by a balloon catheter, dilation of the epicardial coronary artery after reactive hyperemia was markedly attenuated to 7 ± 4 μm (p < 0.01 versus before denudation), despite the presence of a similar degree of reactive hyperemia. The extent of coronary dilation after nitroglycerin was unchanged before and after de-endothelialization. Thus, the endothelium contributed to reactive dilation but not to the nitroglycerin-induced dilation. The negative feedback control of coronary diameter to changes in flow velocity may relate to the regulation of coronary artery tone.