RELEASE OF MARKERS OF MYOCARDIAL AND ENDOTHELIAL INJURY FOLLOWING COLD CARDIOPLEGIC ARREST IN PIGS

Cold cardioplegic arrest causes reperfusion injury to both endothelium and myocardium. We investigated release of troponin-T (TnT), tissue p lasminogen activator activity (t-PA) and histamine (HA) from the heart before and after 2 h of cold crystalloid cardioplegia in eight Swedis h landrace pigs. Coronary sinus blood flow was measured in an external shunt between the coronary sinus and the right atrium. TnT, t-PA and HA were measured concomitantly in arterial and coronary sinus plasma, and the cardiac release was calculated. Cardiac release of TnT increas ed from 18 (15-25) mu g/min (median (central 90% percentile)) before c old cardioplegia to maximum 281 (132-510) mu g/min 30 min after aortic declamping (p < 0.02 vs initial value). t-PA rose from -4 (-52-34) to maximum 249 (75-691) IU/min 2 min after declamping (p < 0.01) and the reafter returned to baseline levels. The net cardiac release of HA was 72 (-80-1321) nmol/min before cardioplegia, rising to 234 (-188-524) after 2 min of reperfusion (p < 0.02) and returning to baseline after 30 minutes. We conclude that the porcine heart releases t-PA, Tn-T and HA during postcardioplegic reperfusion. The differing kinetics of the ir release may indicate different affection of the myocardium and the endothelium. Tn-T, t-PA and HA are potential markers of myocardial and endothelial injury in the porcine heart.