Impaired vasodilatation of epicardial coronary arteries and resistance vessels following myocardial ischemia and reperfusion in anesthetized dogs

To study whether the reactivity of the large coronary artery in vivo is affected by coronary artery occlusion and reperfusion, left circumflex coronary artery diameter, coronary blood flow, systemic arterial blood pressure, and heart rate were measured in anesthetized, open-chest dogs. Intracoronary injections of acetylcholine and glyceryl trinitrate (an endothelium-independent vasodilator) produced increases in both coronary artery diameter (0.06 ± 0.02 mm and 0.15 ± 0.02 mm, respectively) and coronary blood flow (58±15 mL/min and 50 ± 11 mL/min, respectively) under control conditions. Neither arterial blood pressure nor heart rate was affected by the vasodilators. After 60 minutes of coronary artery occlusion and 30 minutes of reperfusion, baseline coronary artery diameter and coronary blood flow were reduced (P P<0.05), whereas glyceryl trinitrate-induced relaxation was not affected. Thus, coronary artery occlusion and reperfusion attenuate endothelium-dependent and -independent dilatation of large coronary arteries and coronary resistance vessels in vivo, whereas only endothelium-dependent relaxation is inhibited in isolated arterial ring experiments. Thus, endothelial dysfunction is not the only factor contributing to reduced vasodilator responses after ischemia and reperfusion. The ischemia-induced constriction of the coronary circulation may restrict the responsiveness to exogenous vasodilators. Also, reduced vasodilator reserve caused by capillary plugging may contribute to the attenuation of the normal increases in coronary blood flow produced by both endothelium-dependent and -independent vasodilators.