Reactive hyperemia (RH) was produced after short-term (5-30 s) cessation of blood flow in experiments on anesthetized dogs following catheterization of the circumflex branch of the left coronary artery (with the chest intact) autoperfused with blood from the subclavian artery. The increase of the coronary blood flow observed after occlusion was shown to depend strictly on its duration. Deendothelization of coronary vessels decreased the RH significantly. In coronary bed the infusion of L-arginine was accompanied by an increase of RH and endothelium-dependent acetylcholine-induced vasodilation. L-arginine produced its effect only when the endothelium was intact, whereas NO synthase inhibition substantially decreased the RH and vasodilating response to intracoronary administration of acetylcholine. It was concluded that the RH was endothelium-dependent and that nitric oxide of endothelial origin was the active humoral component of this reaction.
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