Crystalloid cardioplegia and hypothermia do not impair endothelium-dependent relaxation or damage vascular smooth muscle of epicardial coronary arteries.

Canine hearts were arrested with crystalloid cardioplegic solution (45 minutes at 7 degrees C) to determine whether either cardioplegia or hypothermia impairs the production of endothelium-derived relaxing factor or damages the vascular smooth muscle of epicardial coronary arteries. In addition, isolated coronary artery segments were exposed to either cold (7 degrees C) or warm (37 degrees C) crystalloid cardioplegic solution and physiologic salt solution in vitro for 45 minutes. After cardiac arrest or incubation with the solutions, segments of epicardial coronary artery were prepared and studied in organ chambers. Cardioplegic arrest of the heart or exposure to cardioplegic solution in vitro (7 degrees or 37 degrees C) did not alter endothelium-dependent relaxation of epicardial coronary artery segments in response to adenosine diphosphate or acetylcholine (10(-9) to 10(-4) mol/L). Cardioplegic arrest did not alter G protein-mediated, endothelium-dependent relaxation in response to sodium fluoride. In addition, smooth muscle contraction in response to potassium ions (voltage-dependent) or prostaglandin F2 alpha (receptor-dependent) and relaxation in response to isoproterenol (cyclic adenosine monophosphate-mediated) or sodium nitroprusside (cyclic guanosine monophosphate-mediated) was unaltered after exposure to cardioplegic solution or hypothermia. These experiments demonstrate that hyperkalemic crystalloid cardioplegia does not irreversibly alter function of epicardial coronary arteries. We hypothesize that coronary artery endothelial cell dysfunction identified in previous studies of cardioplegia may have been due to the effects of barotrauma or shear stress on the vasculature and not the effect of cardioplegia per se.