RELEASE OF CREATINE-KINASE, TROPONIN-T, AND TISSUE-PLASMINOGEN ACTIVATOR IN ARTERIAL AND CORONARY VENOUS-BLOOD DURING CORONARY-ARTERY BYPASS-SURGERY

Tissue plasminogen activator (t-PA) as a possible marker of endothelia l injury during elective coronary artery bypass surgery was studied. T -PA antigen and activity were measured in arterial and coronary venous plasma in 14 patients, and compared to the markers of myocyte injury creatine kinase (CK-MB) and troponin-rr (TnT). Cardiopulmonary bypass (CPB) lasted 86 (55-107) min, and aortic cross-clamping (cold, crystal loid cardioplegia) lasted 41 (25-62) min (median (central 90% percenti le)). Blood flow in the great cardiac vein was measured by retrograde thermodilution, and increased from 49 (27-90) ml/min before CPB to a m aximum of 92 (55-125) ml/min 40 min after declamping (not significant) . CK-MB, TnT, and t-PA antigen and activity all increased during CPB, and were significantly higher in coronary sinus than arterial plasma a fter declamping the aorta. Net cardiac release ([coronary sinus - arte rial concentration] x coronary flow) of TnT increased after the aorta was declamped, and was higher in the seven patients with the longest c ross-clamping time than in the seven with the shortest time (p<0.01). Cardiac release of CK-MB and t-PA antigen also increased after declamp ing, but with no significant difference between long and short cross-c lamp times. t-PA activity, however, increased more in the patients wit h the longest cross-clamp times (p<0.008). In conclusion, CK-MB, TnT a nd t-PA were released from the postcardioplegic heart. Release of t-PA indicates that postcardioplegic coronary endothelial activation or in jury occurred. t-PA activity as well as TnT increased more in patients with long times of cross-clamping, indicating that t-PA activity may be a possible marker of postcardioplegic endothelial injury or activat ion.