CHANGES IN COAGULATION AND FIBRINOLYTIC PARAMETERS CAUSED BY EXTRACORPOREAL-CIRCULATION

During cardiopulmonary bypass (CPB) mechanical stress and the contact of blood with artificial surfaces lead to the activation of pro- and a nticoagulant systems and the complement cascade, and to changes in cel lular components. This phenomenon causes the ''postperfusion-syndrome' ', with leukocytosis, increased capillary permeability, accumulation o f interstitial fluid, and organ dysfunction. In this study, we focused on the influence of the extracorporeal circulation, sternotomy, and h eparin administration on the activation of coagulation and fibrinolysi s. In 15 patients we investigated coagulation parameters before, durin g and post CPB, i.e., fibrinogen, antithrombin (AT) III, thrombin-anti thrombin complex (TAT), prothrombin fragments F1 + 2 (F1 + 2), factor (F) XIIa, tissue factor (TF), and parameters of the fibrinolytic syste m, i.e., plasmin-antiplasmin-complex (PAP), D-dimer, tissue-plasminoge n-activator (tPA), urokinase-type plasminogen activator (uPA), and pla sminogen-activator inhibitor type 1 (PAI 1). The results demonstrate d istinct alterations in the above mentioned parameters. Despite adminis tration of a high dose of heparin (activated clotting time [ACT] > 450 s) combined with a low dose of aprotinin, activation of the coagulati on and fibrinolytic pathways was observed. We found this activation wa s mainly caused by CPB and not by sternotomy. The activation of coagul ation was due to foreign surface contact (F XII double right arrow F X IIa) as well as to an effect of tissue factor release in the late phas e of CPB. The enhanced fibrinolytic activity during CPB was, at least in part, caused by tPA and was followed by PAI 1 release.