Cardiopulmonary bypass triggers a generalized inflammatory response that is largely mediated by activation of polymorphonuclear neutrophils, their adhesion to endothelial cells, and the subsequent release of cytotoxic products. It has been known for several years that the inflammatory response to extracorporeal circulation underlies the occasional development of postoperative organ--in particular, lung--dysfunction. It is now increasingly recognized that this response can adversely affect myocardial function as well. These harmful effects are exerted by a wide spectrum of compounds, regardless of whether they act as triggers (complement-derived anaphylatoxins), mediators (cytokines, adhesion molecules), or effectors (proteolytic enzymes, oxygen free radicals, leukotrienes) of the inflammatory cascade. These considerations suggest that future strategies of myocardial protection must not be limited to interventions targeted at the heart itself but should also encompass those designed to blunt the inflammatory response to cardiopulmonary bypass.