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Review examines conventional and novel mechanisms of aprotinin during cardiopulmonary bypass, highlighting pathways that modulate clotting and inflammation.
Induction of the coagulation and inflammatory cascades can cause multiorgan dysfunction after cardiopulmonary bypass (CPB). In light of these observations, strategies that can stabilize the coagulation process as well as attenuate the inflammatory response during and after cardiac surgery are important. Aprotinin has effects on hemostasis. In addition, aprotinin may exert multiple biologically relevant effects in the context of cardiac surgery and CPB. For example, it decreases neutrophil and macrophage activation and chemotaxis, attenuates release and activation of proinflammatory cytokines, and reduces oxidative stress. Despite these perceived benefits, the routine use of aprotinin in cardiac surgery with CPB has been called into question. In this review, we examined this controversial drug by discussing the classical and novel pathways in which aprotinin may be operative in the context of cardiac surgery.
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McEvoy et al. (2007) studied this question.
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