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Ann Thorac Surg 1994;57:1522-1525
© 1994 The Society of Thoracic Surgeons


Articles

Blood cardioplegia reduces oxidant burden in the ischemic and reperfused human myocardium

Domenico Lapenna, MD*, Andrea Mezzetti, MD, Sergio De Gioia, MD, Sante D. Pierdomenico, MD, Anna Maria Verna, Franca Daniele, MD, Leonardo Marzio, MD, Carmine Di Ilio, PhD, Antonio Maria Calafiore, MD, Franco Cuccurullo, MD

Istituto di Fisiopatologia Medica and Cattedra di Cardiochirurgia, Universita' "G. D'Annunzio," Facolta' di Medicina e Chirurgia, Chieti, Italy

Accepted for publication September 30, 1993.

* Address reprint requests to Dr Lapenna, c/o Presidenza Fscolta' di Medidna e Chirurgia, Via del Vestini, 66100 Chieti, Italy.

In 20 patients receiving cold crystalloid caidioplegia (n = 10) or cold blood cardioplegia (n = 10) during elective coronary artery bypass grafting, the atrial myocardium was tested for glutathione-related antioxidant defenses and lipid pemxidation. In both groups, ischemia and reperfusion induced a significant increase in lipid peroxdation values (p < 0.05) that was associated with a depression of nonprotein thiol compound levels (p < 0.05). Compared with the cold crystalloid cardioplegiatreated patients, the cold blood cardioplegia-treated patients showed a lower lipid peroxidation (p < 0.05) and higher values of nonprotein thiol compounds (p < 0.05). Moreover, a significant ischemia and reperfusiondependent activation of glutathione transferase was oberved only in the cold crystalloid cardioplegia-treated patients. Selenium-dependent glutathione peroxidase and glutathione reductase activities did not change after release of the aortic cross-clamp and did not differ between the two groups. The highest postoperative plasma level of the myocardial-spetific isoenzyme of creatine kinase was significantly more elevated in the cold crystalloid cardioplegia patients. Overall, these tissue biochemical features indicate a lower oxidanl burden in the myocardium of cold blood cardioplegia-treated patients, a finding suggesting superior protection for the ischemic and reperfused human myocardium also through antioxldant-type mechanisms, apparently mediated by the antioxidant capacity of erythrocytes and specific plasma molecules.




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