Aprotinin complements heparin bonding in an in vitro model of cardiopulmonary bypass

The relative contribution of full‐dose aprotinin, used with heparin‐bonded surfaces, to contact activation during cardiopulmonary bypass was examined. In vitro Carmeda‐bonded cardiopulmonary bypass circuits were perfused with whole blood anticoagulated with heparin (3.3 U/ml). Aprotinin (300 kIU/ml) was added to the circuits of one set of experiments. Samples were taken prior to perfusion and at 30, 60, 120 and 360 min. The activated coagulation time was extended in the aprotinin experiments, significantly at 30 min ( P  = 0.003) and 120 min ( P  = 0.001). Thrombin–antithrombin complexes and prothrombin fragment F1+2 were both higher in the non‐aprotinin experiments at 120 min ( P  = 0.02 each) and 360 min ( P  = 0.005 and 0.001, respectively). Plasma leucocyte elastase was raised in the non‐aprotinin experiments in comparison to the aprotinin experiments at each timepoint (30 min, P  = 0.04; 60 min, P  = 0.006; 120 min, P  = 0.001; 360 min, P  = 0.0001), as was interleukin‐8 at 120 min ( P  = 0.05) and 360 min ( P  = 0.0001). No differences were found for the platelet activation marker P‐selectin. Platelet and white blood cell counts fell significantly in the non‐aprotinin experiments compared with the aprotinin experiments at 360 min ( P  = 0.05 and 0.03, respectively). It would appear that the use of aprotinin has additional haemostatic beneficial effects to those found with heparin‐bonded circuits in terms of effects on contact activation and inflammation.