The occurrence of SIRS in patients undergoing CPB has led to the development of strategies designed to prevent or to minimize its occurrence. Many reports have focused on the increased serum concentrations of cytokines (eg, IL-2R, IL-6, IL-8, tumor necrosis factor alpha) and other modulators of inflammation (eg, P-selectin, sE-selectin, soluble intercellular adhesion molecule-1, plasma endothelial cell adhesion molecule-1, and plasma malondialdehyde), which reflect leukocyte and platelet activation, in triggering the onset of SIRS. A study showed a greater upregulation of neutrophil CD11b expression (a marker of leukocyte activation) in patients who sustained a 50% increase in the serum creatinine concentration after CPB, thereby implicating acti- vated neutrophils in the pathophysiology of SIRS and the occurrence of post-CPB renal dysfunction.62 Modulating neutrophil activation to reduce the occurrence of SIRS has been investigated; however, the results have been inconsis- tent. Preoperative intravenous methylprednisolone (10 mg/ kg) caused a reduction in the serum concentrations of many of these cytokines after CPB, but this reduction was not associ- ated with improved hemodynamic variables, diminished blood loss, less use of inotropic agents, shorter duration of ventilation, or shorter ICU length of stay.63 Similarly, the use of intravenous immunoglobulin G in patients with post-CPB SIRS has not been associated with decreased rates of short- term morbidity or 28-day mortality.64 Other strategies to mitigate the occurrence of SIRS after CPB have been evaluated, including the use of 1) CPB circuits (including oxygenators) coated with materials known to reduce complement and leukocyte activation; 2) CPB tubing that is covalently bonded to heparin; and 3) CPB tubing coated with polyethylene oxide polymer or Poly (2-methoxyethylacrylate). 