The inflammatory response to cardiopulmonary bypass is the product of a complex interplay of humoral and cellular components. Contact activation cascades, the complement system, and cytokines comprise the humoral elements and interact in such a way as to propagate their own cascades and to activate the cellular elements. Neutrophils and endothelial cells are the cellular components and become involved after their "activation" by the humoral mediators. Neutrophil-endothelial cell adherence is the initial step of the cellular inflammatory response and is promoted by the expression of specific adhesion molecules on the surfaces of both of these cells leading to the emigration of neutrophils into the extravascular space where they release toxins that damage surrounding tissues. The resulting organ dysfunction produces the clinical picture referred to as the "postperfusion syndrome." Strategies to attenuate this response include the administration of corticosteroids, aprotinin, and anticytokine monoclonal antibodies, as well as various modifications of the bypass circuit. The existence of multiple pathways to trigger this inflammatory response hampers efforts at its attenuation and leaves much investigation to be done as the quest to understand the body's inflammatory response to cardiopulmonary bypass continues.