BACKGROUND: Left ventricular dysfunction is frequently observed in patients after hypothermic cardioplegic arrest, and often inotropic intervention is necessary for patients to be successfully weaned from cardiopulmonary bypass (CPB). A myocardial beta-adrenergic receptor (beta AR) desensitization has been noted to occur after hypothermic CPB in patients undergoing coronary artery bypass grafting. This randomized study was undertaken to determine the effect of cardioplegic solution temperature on cardiac beta ARs. METHODS: Two groups of patients (20 patients in each) scheduled for elective coronary artery bypass grafting underwent CPB with either intermittent warm or cold blood cardioplegia. The density of the beta ARs, the proportion of beta 1- to beta 2-adrenergic receptors, and the beta AR coupling capacity to adenylate cyclase were determined in specimens of the right atrial tissue at baseline, during CPB, and after discontinuation of CPB. Plasma concentrations of catecholamines were also measured in both arterial and coronary sinus samples. RESULTS: In both cardioplegia groups, no significant modification in either the beta AR density or the proportion of beta 1- to beta 2-adrenergic receptors was detected. However, a significant decrease in adenylate cyclase activity after stimulation with isoproterenol was observed in the cold blood cardioplegia group during CPB (p < 0.01) and 30 minutes after its discontinuation (p < 0.05). Moreover, a significant decrease in adenylate cyclase activity during CPB was detected in this group after stimulation with sodium fluoride (p < 0.05), but this pattern was found to be completely reversed by 30 minutes after discontinuation of CPB. No modification in the basal or stimulated adenylate cyclase activity was observed in the warm blood cardioplegia group during or after CPB. CONCLUSIONS: Our results confirm the finding from previous studies of a cardiac beta AR desensitization after hypothermic cardioplegic arrest, and provide evidence of the advantages of intermittent warm blood cardioplegia in preserving the autonomic sympathetic function of the heart.