Release of Markers of Myocardial and Endothelial Injury Following Cold Cardioplegia Arrest in Pigs

Abstract

Cold cardioplegic arrest causes reperfusion injury to both endothelium and myocardium. We investigated release of troponin-T (TnT), tissue plasminogen activator activity (t-PA) and histamine (HA) from the heart before and after 2 h of cold crystalloid cardioplegia in eight Swedish 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 increased from 18 (15–25) μg/min (median (central 90% percentile)) before cold cardioplegia to maximum 281 (132–510) μg/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 thereafter 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 their 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.

Key Words:

• cardioplegia
• histamine
• pig
• troponin-T
• tissue plasminogen activator