Reperfusion after cardioplegic cardiac arrest--effects on intracoronary leucocyte elastase release and oxygen free radical mediated lipid peroxidation.

In experimental animal models reperfusion of ischaemic myocardium causes sequestration of leucocytes within the coronary circulation. Leucocytes contribute to postischaemic myocardial injury by releasing proteolytic enzymes and by generating oxygen free radicals. The aim of this study was to investigate whether leucocytes also contribute to myocardial injury following ischaemia and reperfusion associated with cardioplegic cardiac arrest. Therefore, we studied the release of the proteolytic enzyme elastase and oxygen free radical initiated myocardial lipid peroxidation in coronary sinus blood during reperfusion after cardioplegic cardiac arrest. The elastase-alpha-1-proteinase inhibitor complex and malondialdehyde (a byproduct of myocardial lipid peroxidation) were measured in arterial, central venous and coronary sinus blood samples in 19 patients undergoing elective coronary artery bypass grafting before aortic crossclamping and 1, 5, 10 and 20 m in after aortic declamping. Malondialdehyde concentrations did not increase significantly during the study period, whereas elastase concentrations showed a significant increase during cardiopulmonary bypass in arterial, central venous as well as coronary sinus blood. Neither elastase nor malondialdehyde concentrations in coronary sinus blood differed significantly from arterial or central venous blood at any time point measured. Our data demonstrated increased elastase concentrations during cardiopulmonary bypass, but we did not find enhance intracoronary elastase release or myocardial during cardiopulmonary bypass, but we did not find enhanced intracoronary elastase release or myocardial lipid peroxidation. Our data suggest that patients are sufficiently protected from leucocyte mediated ischaemia reperfusion injury during uncomplicated coronary artery bypass grafting with cardioplegic arrest.