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Abstract
Cardiopulmonary bypass (CPB)is associated with a significant inflammatory reaction characterized by complement activation, liberation of end toxin, cellular activation, free radical production and release of cytokines and other mediators (nitric oxide). Chemo tactic cytokines, especially IL-6, play a major role in the activation of the inflammatory cascade. Activation of the contact system leads to generation of kallikerin, which in turn leads to plasmid formation and activation of coagulation. This inflammatory response is associated with an anti-inflammatory response, including the release of IL-10 and tumor necrosis (TNF) receptors. The predominant inflammatory reaction might contribute to postoperative complications, including the development of postoperative myocardial or other organ dysfunction. Different strategies for reducing the inflammatory reaction have been proposed, including the administration of corticosteroids, apportioning and antioxidants. Also the use of leukocyte depletion filters, heparin coated surfaces in the CPB circuits, and even the use of off-pump surgical techniques .