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Ann Thorac Surg 2006;82:2315-2322
© 2006 The Society of Thoracic Surgeons
Harrison Department of Surgical Research, School of Medicine, University of Pennsylvania, and The Sol Sherry Thrombosis Research Center, Hematology Division, Department of Medicine, Temple University, Philadelphia, Pennsylvania
* Address correspondence to Dr Edmunds, 3440 Market St, Suite 306, Philadelphia, PA 19104-3325 (Email: hank.edmunds{at}uphs.upenn.edu).
Cardiopulmonary bypass (CPB) ignites a massive defense reaction that stimulates all blood cells and five plasma protein systems to produce a myriad of vasoactive and cytotoxic substances, cell-signaling molecules, and upregulated cellular receptors. Thrombin is the key enzyme in the thrombotic portion of the defense reaction and is only partially suppressed by heparin. During CPB, thrombin is produced by both extrinsic and intrinsic coagulation pathways and activated platelets. The routine use of a cell saver and the eventual introduction of direct thrombin inhibitors now offer the possibility of completely suppressing thrombin production and fibrinolysis during cardiac surgery with CPB.
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