Coronary Arteries In Vivo

a specific inhibitor, the hypothesis that acetylcholine-induced coronary vasodilation is due to EDRF release was tested. Methods and Results. We studied the response of normal coronary arteries to acetylcholine (an endothelium-dependent vasodilator) and isosorbide dinitrate (an endothelium-independent vasodilator) in seven patients. The specificity of any vasodilator response was assessed by the infusion of reduced free human hemoglobin. Hemoglobin 10M infusion alone had no effect on coronary artery diameter. Drugs were infused into the coronary artery, and the diameter changes were assessed by quantitative angiography. Acetylcholine 10M increased left anterior descending coronary artery diameter from control: 230±0.12 mm to 2.79±0.20 mm (mean+SEM, n=7, p<0.01). Hemoglobin both in a concentration of 10` M and 10` M reversed this vasodilator effect, causing constriction to 2.11±0.18 mm (p<0.001 compared with acetylcholine 10M) and 2.29±0.14 mm (p<0.05 compared with acetylcholine 10M). Isosorbide dinitrate in the presence of hemoglobin caused dilatation of the coronary artery in all cases to 3.04±0.24 mm (p<0.001 compared with acetylcholine 10` M and hemoglobin 10-6 M). Conclusions. Using a specific inhibitor of nitric oxide, reduced free hemoglobin, we have demonstrated that basal EDRF release does not appear to play an important role in the maintenance of human epicardial coronary artery diameter in vivo but is responsible for the acetylcholine-induced dilatation. (Circulation 1993;87:80-85)