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Ann Thorac Surg 1993;55:1546-1552
© 1993 The Society of Thoracic Surgeons

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Articles

Efflux of adenosine and its catabolites during cold blood cardioplegia

^a Departments of Cardiothoracic Surgery, Anesthesiology, and Internal Medicine, Oulu University Central Hospital Finland
^b Department of Medical Biochemistry, Oulu University, Oulu, Finland

Accepted for publication October 7, 1992.

^_* Address reprint requests to Dr Peuhkurinen, Division of Cardiology, Department of Internal Medicine, Oulu University Central Hospital, Kajaaninlie 50, 90220 Oulu, Finland.

Levels of myocardial high-energy phosphates decrease during cardioplegia for open heart operations, with a subsequent increase in the level of adenosine and its metabolites. It has been demonstrated in experimental models that the effluent concentrations of purines can be used as a measure of the average myocardial energy state. Net adenylate loss and myocardial energy state were evaluated here by determining aorta-coronary sinus differences in levels of adenosine catabolites in 17 patients during cold blood cardioplegia for elective coronary artery bypass grafting. Repeated blood samples were taken before cross-clamping of the aorta, when cardioplegic solute was infused into the aortic root and grafts after five distal anastomoses, and after declamping of the aorta. The aorta-coronary sinus differences in levels of total purines increased 4.7-, 7.5-, 7.1-, 7.8-, and 10.2-fold (from the preclamp level of 1.7 ± 0.7 µmol/L; p < 0.001) for grafts one through five anastomosed at an average of 19, 34, 50, 63, and 76 minutes after the aortic cross-clamp, respectively. Hypoxanthine and xanthine were present in the highest concentrations. Vasodilatory adenosine concentrations of 1 to 2 µmol/L were observed in the coronary sinus while the aorta was cross-clamped. There was a linear positive correlation between the aorta-coronary sinus purine differences and corresponding cross-clamp time (r = 0.62; p < 0.001). The metabolite differences settled at a more negative level after declamping of the aorta than that prevailing before placement of the cross-clamp, suggesting continuous washout of adenosine and its catabolites during the 30-minute postclamp observation period. We conclude that considerable net efflux of purines occurs even during cold blood cardioplegia, the relative changes in effluent concentrations being greatest at the very beginning and toward the end of the cross-clamp time. The net loss of high-energy phosphates may be of some clinical significance in the development of postoperative myocardial stunning, especially with prolonged aortic cross-clamp times. On the other hand, monitoring efflux of adenosine and its catabolites into the coronary sinus during and after aortic cross-clamping could be used for comparing different cardioplegia methods.

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