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PHILIP J. HESS, JR., M.D., is Assistant Professor, University of Florida and Shands Hospital, 1600 SW Archer Road, Gainesville, FL 32610-0286 (hesspj{at}surgery.ufl.edu).

Purpose. Several aspects of the systemic inflammatory response to coronary artery bypass graft surgery are described. Summary. The inflammatory response is a fundamental biological protective mechanism that gathers together the body’s cellular and chemical defense mechanisms at the local site of tissue injury. The systemic inflammatory response syndrome refers to a systemic, whole body, non-localized response. This response, which occurs to some degree in most patients undergoing coronary artery bypass graft surgery, has the potential to affect all tissues and vital organs. When blood interacts with the cardiopulmonary bypass machine, several cellular and humoral pathways are activated including the complement system, the coagulation system, and the fibrinolytic system. These, in turn, activate inflammatory response cells, such as leukocytes and platelets. Together these molecular pathways and activated cells mediate the frequently observed clinical sequelae such as edema, tissue and organ damage, and hyperfibrinolysis. In order for a molecule drug to attenuate effectively this response, it would need to have a broad enough spectrum of activity to inhibit multiple pathways and to limit their cross-amplification. Aprotinin, a nonspecific serine protease, is an important attenuator of this response as it inhibits several important serine proteases, including kallikrein, plasmin, thrombin, and elastase, which are involved in fibrinolysis and cell transmigration and degranulation into soft tissues. Conclusion. Treatment with aprotinin during coronary artery bypass graft surgery should be considered as a way to attenuate bleeding and systemic inflammatory responses. Index terms: Aprotinin; Coronary artery bypass; Hemostatics; Mechanism of action