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Pasquale Mastroroberto
Vincenzo De Amicis
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Ann Thorac Surg 1997;63:683-688
© 1997 The Society of Thoracic Surgeons


Original Article: Cardiovascular

Intermittent Warm Blood Cardioplegia Preserves Myocardial ß-Adrenergic Receptor Function

Massimo Chello, MD, Pasquale Mastroroberto, MD, Vincenzo De Amicis, MD, Donato Pantaleo, MD, Raimondo Ascione, MD, Nicola Spampinato, MD

Department of Cardiac Surgery, Medical School of Catanzaro, Catanzaro, and Department of Cardiac Surgery, Medical School of Naples, Naples, Italy

Accepted for publication October 5, 1996.

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 ß-adrenergic receptor (ßAR) 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 ßARs.

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 ßARs, the proportion of ß1- to ß2-adrenergic receptors, and the ßAR 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 ßAR density or the proportion of ß1- to ß2-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 ßAR 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.




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