| Backround: Postoperative lung injury is one of the most frequent complications of cardiac surgery that impacts significantly on health-care expenditures and largely has been believed to result from the use of cardiopulmonary bypass (CPB). CPB has been shown to induce complement activation, endotoxin release, leukocyte activation, the expression of adhesion molecules, and the release of many inflammatory mediators including oxygen-free radicals, arachidonic acid metabolites, cytokines, platelet-activating factor, nitric oxide, and endothelins. Therapies aimed at interfering with the inflammatory response include the administration of pharmacologic agents such as corticosteroids, aprotinin, and antioxidants, as well as modification of techniques and equipment by the use of heparin-coated CPB circuits, intraoperative leukocyte depletion, and ultrafiltration. Improved understanding of the inflammatory reactions to CPB can lead to improved patient outcome by enabling the development of novel therapies aimed at limiting this response. However, recent comparative studies between conventional and off-pump coronary artery bypass grafting have indicated that CPB itself may not be the major contributor to the development of postoperative pulmonary dysfunction. Recent study of the inflammatory reactions occurring during and after CPB has improved our understanding of the involvement of the inflammatory cascade in perioperative injury. The exact... |