APROTININ INHIBITS THE CONTACT, NEUTROPHIL, AND PLATELET ACTIVATION SYSTEMS DURING SIMULATED EXTRACORPOREAL PERFUSION

Aprotinin reduces blood loss after cardiac operations and decreases th e bleeding time. The mechanism of action of aprotinin that produces th ese effects is not clear. During simulated extracorporeal circulation the contact and complement systems, platelets, and neutrophils are act ivated. We investigated the effect of aprotinin on kallikrein-C1BAR-in hibitor complex and C1BAR-C1BAR-inhibitor complex formation, neutrophi l degranulation, and platelet release and aggregation during simulated extracorporeal circulation. Fresh heparinized human blood was recircu lated at 37-degrees-C for 2 hours in a spiral coil membrane oxygenator -roller pump perfusion circuit. Changes in platelet count, leukocyte c ount, platelet response to adenosine diphosphate, and plasma levels of beta-thromboglobulin, kallikrein-C1BAR-inhibitor complexes, C1BAR-C1B AR-inhibitor complexes, and neutrophil elastase were measured before a nd at 5, 30, 60, and 120 minutes of recirculation at 0, 0.015, 0.03, 0 .06, and 0.12 mg/ml doses of aprotinin.