CHANGES IN THE CONTACT SYSTEM DURING ORTHIOTOPIC LIVER-TRANSPLANTATION WITH AND WITHOUT APROTININ

The main cause of nonsurgical bleeding during orthotopic liver transpl antation has been attributed to be hyperfibrinolysis due to high plasm a levels of tissue plasminogen activator. The aim of this study was to investigate contact activation and its possible contribution to fibri nolysis during OLT with and without aprotinin. Aprotinin or placebo wa s given to 20 patients undergoing OLT as part of a randomized double-b lind trial. Plasma samples were collected before, during, and after OL T. There were decreased preoperative levels of prekallikrein and facto r XIIa (P<0.05), with a trend for kallikrein and factor XIIa activity to increase during OLT peaking on reperfusion (P<0.05). Kallikrein inh ibition, C1 esterase inhibitor, and alpha-2-macroglobulin levels were normal before surgery, with low normal levels of antithrombin III and alpha-2-antiplasmin; these levels decreased during OLT with no specifi c change on reperfusion. In the aprotinin-treated group, kallikrein in hibition levels increased (P<0.05) from preoperative mean (+/- SD) val ues of 101+/-47% to 154+/-42% and antiplasmin levels increased (P<0.05 ) from 72+/-28% to 243+/-53% during the anhepatic phase, reflecting th e effect of aprotinin. The antifibrinolytic effect of aprotinin was de monstrated by decreased levels of D-dimer on reperfusion (P<0.05) and at the end of OLT (P<0.001) in the aprotinin-treated group. We have sh own that contact activation during OLT is minimal and that aprotinin d oes not alter the pattern of contact activation, but provides an antik allikrein effect.