Inflammatory response to cardiopulmonary bypass

Cardiac surgery with the use of cardiopulmonary bypass (CPB) is associated with an inflammatory process in which activated leukocytes and endothelial cells play a central role. Recent observations indicate that complement act ivation, along with the release of many mediators, such as endotoxin, cytok ines, and neutrophil adhesion molecules, is critical in inducing the activa tion of leukocytes and endothelial cells during CPB. Moreover, some proinfl ammatory cytokines can be released locally from the heart, which may enhanc e leukocyte activation as well as leukocyte accumulation in the ischemic-re perfused myocardium. For instance, it has been found that postoperative lev els of cardiac troponin-I, a highly specific marker of myocardial injury, c orrelate strongly with interleukin-8 values in patients undergoing coronary artery bypass grafting. Consequently, avoiding the use of CPB or improving the biocompatibility of CPB may lead to improved patient recovery. An off- pump approach is associated with reduced cytokine production compared with the conventional. approach, which itself can diminish the degree of myocard ial injury. Reduced inflammatory reactions with a lesser degree of myocardi al injury have also been discovered following steroid pretreatment and with the use of heparin-coated CPB circuits. The balance between the pro- and a nti-inflammatory response may be crucial in limiting the extent of inflamma tory injury The continued explosion in molecular biological knowledge will help to develop ideal therapies to restrict the inflammatory response and i ts subsequent damaging effects.