Prevention of blood activation during and complications after cardiopulmonary bypass

The cardiopulmonary bypass (CPB) circuit for open heart surgery initiates a whole body inflammatory reaction (WBIR) resulting in impaired hemostasis and organ dysfunction. Impaired hemostasis appeared to be related to the activation of the contact system (factor XII), which can be inhibited by protease inhibitors like aprotinin, resulting in preserved hemostasis. The primary effect of aprotinin is the inhibition of the kinin, fibrinolytic and, synergetically with heparin, the clotting system. However, the hemostatic effect seems to be related to the platelet receptors associated with cell adhesion (GpIb), which are affected in the first 5 minutes of bypass but are preserved by aprotinin. Organ dysfunction is related to activation of the complement system, which triggers a leukocytory inflammatory reaction, which can be inhibited by corticosteroids. This inflammatory reaction is associated with TNF release, particularly manifest after release of the aortic crossclamp. The use of heparin coated (Duraflo II) CPB circuits reduced the activation of the clotting system. The combination of drug treatment with coated circuits might reduce or even prevent the induction of the whole body inflammatory reaction by the CPB circuit and so the inherent postoperative complications