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Abstract :
[en] During heart surgery, several humoral cascades (coagulation, complement, kallicrein-kinin, cytokines, fibrinolysis) and several cell systems (platelets, neutrophils, endothelial cells, ...) are activated. Numerous contributing factors have been reported: blood contact with foreign surfaces of the extracorporeal circuits, blood-air interface, lung and myocardial ischemia-reperfusion after unclamping, hypothermia, shear stresses, ... A post-perfusion syndrome may develop which include miscellaneous symptoms: coagulation disturbances and bleeding, neurological alterations, inflammatory syndrome, and, in extreme cases, multisystemic organ failure. Even if the present mortality of cardiac surgery is low, several approaches have been proposed to reduce such activations. They are based on changing in the circuit design, or in the composition of the luminal surfaces of the tubing and oxygenator, on improvement of the operative technique, and on modifications of the perfusion technique. Pharmacological agents are also used (anti-inflammatory drugs, corticoids, serine proteases inhibitor (aprotinin, ...). Nevertheless, the development of more biocompatible surfaces seems a promising goal.
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