RELEASE OF LIPOPOLYSACCHARIDE TOXICITY-MODULATING PROTEINS IN PATIENTS UNDERGOING CARDIOPULMONARY BYPASS USING NONCOATED AND HEPARIN-COATEDEXTRACORPOREAL CIRCUITS - A CLINICAL PILOT-STUDY

Study objective: Cardiopulmonary bypass (CPB) induces a generalized in flammatory response, including activation of leukocytes, contributing to postoperative morbidity. The inflammatory pathways leading to this systemic inflammatory response syndrome are considered identical to th ose involved in septic shock. Therefore, we studied the release of bac tericidal/permeability-increasing protein (BPI), lipopolysaccharide bi nding protein (LBP), and soluble CD14 (sCD14)-all proteins that modula te the effects of lipopolysaccharide (LPS)-in patients undergoing CPB. In addition, the effect of heparin coating of the extracorporeal bypa ss circuit on the release of these parameters was assessed. Design: Pr ospective, randomized clinical pilot study. Setting: Cardiothoracic Su rgery Department in a university hospital. Patients: Fourteen patients undergoing elective coronary artery bypass grafting were included. Se ven patients underwent CPB using a standard, noncoated extracorporeal circuit, and seven patients had CPB using a heparin-coated extracorpor eal circuit (Duraflo II). Interventions: Blood samples were taken afte r induction of anesthesia, just before aortic crossclamping, and 0, 0. 5, 1.5, 3, 6, 12, and 24 h after declamping. Measurements ana results: CPB with a noncoated extracorporeal circuit induced a sharp increase in neutrophil-derived BPI, manifest directly after release of the aort ic crossclamp, which was significantly attenuated using a heparin-coat ed system. Also, CPB induced a gradual increase of the acute-phase rea ctant LBP, which was identical in the noncoated and heparin-coated gro ups. Systemic release of sCD14 after crossclamp release was significan tly higher in the noncoated group compared with the heparin-coated gro up, but did not rise above baseline levels. Conclusions: These data co nfirm that CPB-induced leukocyte activation is attenuated using a hepa rin-treated extracorporeal circuit and point to the possible role of L PS toxicity-modulating proteins in the systemic inflammatory response after bypass surgery.