• Sune Damgaard, Claus H Nielsen, Lars W Andersen, Klaus Bendtzen, Michael Tvede, and Daniel A Steinbrüchel.
• Department of Cardiothoracic Surgery, Rigshospitalet, Copenhagen University Hospital, Copenhagen, Denmark. sunedamgaard@dadlnet.dk
• Ann. Thorac. Surg. 2010 May 1;89(5):1511-7.

BackgroundThis study investigated whether intraoperative use of a cell saver reduces the systemic inflammatory response after coronary operations using cardiopulmonary bypass (CPB).MethodsThe study randomized 29 patients, 15 to cell saving of pericardial suction blood and residual blood in the CPB circuit after perfusion (cell saver group) vs 14 who received direct retransfusion of the suction blood and the CPB circuit blood (control group). Outcome measures were plasma concentrations of the inflammatory markers interleukin (IL)-1beta, IL-6, IL-8, IL-10, IL-12, tumor necrosis factor-alpha, soluble tumor necrosis factor receptors I and II, and procalcitonin at 6, 24, and 72 hours postoperatively.ResultsAt 6 hours postoperatively, the cell saver group displayed significantly reduced plasma levels of IL-6 and IL-8 (p < 0.05). A reduction in IL-10 was also found (p = 0.05), along with nonsignificant reductions in the remaining markers. At 24 and 72 hours, significant differences between groups no longer existed. In the cell saver group, the suction blood and CPB circuit blood were cleared for tumor necrosis factor receptors (p < 0.005), and IL-6, IL-8, IL-10, and procalcitonin were significantly reduced (p < 0.05). Median intraoperative blood loss was 250 mL in the cell saver group vs 475 mL (p < 0.02). Immediately postoperatively the hemoglobin level was higher in the cell saver group (p < 0.03). Transfusion requirements were similar.ConclusionsThe cell saver reduced the systemic levels of the proinflammatory markers IL-6 and IL-8 at 6 hours after CPB. The role of the anti-inflammatory molecules IL-10 and soluble tumor necrosis factor receptors is undefined in this setting.Copyright (c) 2010 The Society of Thoracic Surgeons. Published by Elsevier Inc. All rights reserved.

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