FIBRINOLYSIS DURING CARDIAC-SURGERY - RELEASE OF TISSUE-PLASMINOGEN ACTIVATOR IN ARTERIAL AND CORONARY SINUS BLOOD

Endothelial release of tissue plasminogen activator (t-PA) may initiat e fibrinolysis. Fibrinolysis and coagulation were investigated in 12 p atients undergoing elective coronary artery bypass surgery. Cardiopulm onary bypass (CPB) was 108 +/- 7 min (mean +/- SEM), the time of cold, crystalloid, retrograde cardioplegia 53 +/- 5 min. Arterial and coron ary sinus blood were sampled concomitantly before cardioplegia and aft er release of the aortic cross-clamp, for measurement of t-PA antigen (Ag) and activity, plasminogen activator inhibitor (PAI-1) Ag and acti vity, t-PA/PAI-1 complex, single chain urokinase (sc-uPA) and urokinas e (uPA) plasminogen activators, the fibrin split product D-dimer, thro mbin-antithrombin complex (TAT), and the prothrombin split product F 1 + 2. Cardiopulmonary bypass significantly increased t-PA Ag and activ ity, t-PA/PAI complex, D-dimer, TAT, and F 1 + 2, and decreased PAI-1 Ag and activity in arterial blood; uPA and sc-uPA were unchanged. The tissue plasminogen activator antigen was higher in coronary sinus than arterial blood after 1 (39 +/- 5 vs 24 +/- 4 ng/ml, P < 0.003), 4 (P < 0.003), and 10 min (P < 0.004) reperfusion. Tissue plasminogen activ ator activity and t-PA/PAI complex increased, PAI-1 activity decreased , while all other parameters were unchanged across the coronary circul ation. In conclusion, CPB induces fibrinolysis and coagulation. Cold c ardioplegia induces t-PA release in the coronary circulation, denoting a postischemic antithrombotic function of the coronary endothelium. T issue plasminogen activator may be used to evaluate endothelial stimul ation or injury induced by CPB, or by different regimens of myocardial protection.