To determine whether University of Wisconsin solution impairs production of endothelium-derived relaxing factor or damages vascular smooth muscle function of epicardial coronary arteries, isolated segments of canine left circumflex coronary artery were exposed to either cold (7 degrees C) or normothermic (37 degrees C) University of Wisconsin solution or to cold (30 degrees C) or normothermic (37 degrees C) physiologic salt solution in vitro for 60 minutes. After incubation with the solutions, the vascular segments were studied in vitro in organ chambers. Exposure to cold or to normothermic University of Wisconsin solution did not alter endothelium-dependent relaxation (either maximal relaxation or ED50) of the segments in response to adenosine diphosphate or acetylcholine (10(-9) to 10(-4) mol/L). Also, contraction of the segments in response to potassium ions (voltage-dependent) or prostaglandin F2 alpha (receptor-dependent) and relaxation in response to isoproterenol (cyclic AMP-mediated) or sodium nitroprusside (cyclic GMP-mediated) were unaltered after exposure to cold University of Wisconsin solution. Direct exposure to normothermic University of Wisconsin solution induced transient vasoconstriction in segments with or without endothelium. Thus University of Wisconsin solution does not irreversibly impair release of endothelium-derived relaxing factor or alter function of vascular smooth muscle in epicardial coronary arteries.