ONE-HOUR EXPOSURE TO UNIVERSITY-OF-WISCONSIN SOLUTION DOES NOT IMPAIRENDOTHELIUM-DEPENDENT RELAXATION OR DAMAGE VASCULAR SMOOTH-MUSCLE OF EPICARDIAL CORONARY-ARTERIES

To determine whether University of Wisconsin solution impairs producti on of endothelium-derived relaxing factor or damages vascular smooth m uscle function of epicardial coronary arteries, isolated segments of c anine left circumflex coronary artery were exposed to either cold (7-d egrees-C) or normothermic (37-degrees-C) University of Wisconsin solut ion or to cold (30-degrees-C) or normothermic (37-degrees-C) physiolog ic salt solution in vitro for 60 minutes. After incubation with the so lutions, 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 relaxa tion or ED50) of the segments in response to adenosine diphosphate or acetylcholine (10(-9) to 10(-4) mol/L). Also, contraction of the segme nts in response to potassium ions (voltage-dependent) or prostaglandin F2alpha (receptor-dependent) and relaxation in response to isoprotere nol (cyclic AMP-mediated) or sodium nitroprusside (cyclic GMP-mediated ) were unaltered after exposure to cold University of Wisconsin soluti on. Direct exposure to normothermic University of Wisconsin solution i nduced transient vasoconstriction in segments with or without endothel ium. Thus University of Wisconsin solution does not irreversibly impai r release of endothelium-derived relaxing factor or alter function of vascular smooth muscle in epicardial coronary arteries.