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Reduced pulmonary inflammatory response during cardiopulmonary bypass: effects of combined pulmonary perfusion and carbon monoxide inhalation

^a Department of Anesthesiology and Critical Care Medicine, University Medical Center Freiburg, Germany
^b Department of Cardiovascular Surgery, University Medical Center Freiburg, Hugstetterstrasse 55, D-79106 Freiburg, Germany
^c Department of Cardiovascular Surgery, University of Leipzig, Germany

Received 25 September 2007; received in revised form 20 June 2008; accepted 2 July 2008.

^_* Corresponding author. Tel.: +49 761 270 2825; fax: +49 761 270 2550. (Email: Christian.schlensak{at}uniklinik-freiburg.de).

Objective: Pulmonary inflammation induced by cardiopulmonary bypass (CPB) is one of the main causes for lung injury after cardiac surgery. Pulmonary perfusions as well as carbon monoxide (CO) inhalation are known to reduce the inflammatory reaction of the lung. We hypothesized that a combination of pulmonary perfusion and carbon monoxide inhalation leads to an even stronger reduction of the lung inflammation. Methods: Pigs (n = 7 per experimental group) were randomized to sham operation (SHAM), conventional CPB (CPB), inhalation of CO (CPB + CO, 250 ppm), pulmonary perfusion (CPB + PP) or pulmonary perfusion plus inhalation of CO (CPB + PP + CO). Various cytokine levels (TNF-, IL-1, IL-6, and IL-10) and caspase-3 activity were measured using enzyme-linked immunosorbent assay (ELISA). Transcription factor activity was analyzed via electrophoretic mobility shift assay (EMSA). Blood gases and hemodynamics were measured continuously. A p value <0.05 assessed by Holm–Sidak method was considered statistically significant. Results: Hemodynamic parameters and blood gas analysis showed no significant differences between the groups. While IL-1 protein expression was comparable between the groups, TNF- (478 ± 58 vs 869 ± 95 pg/ml; p < 0.001) and IL-6 protein levels in the lung (256 ± 82 vs 936 ± 76 pg/ml; p < 0.001) showed a significant inhibition in the CPB + PP + CO group at 120 min post-bypass time compared to the CPB group. The cytokine levels were comparable to the CPB + PP and CPB + CO group. IL-10 protein expression (325 ± 47 vs 65 ± 27 pg/ml; p < 0.05) was significantly higher in the CO-treated compared to CPB + PP and CPB-treated animals at 120 min post-bypass. Activation of the transcription factors NF-B and AP-1 showed a CO-mediated induction compared to the CPB or CPB + PP group. Caspase-3 activity revealed a CO-dependent, significant inhibition in CO and CPB + PP + CO-treated animals compared to CPB animals (p < 0.05). Conclusion: The combination of pulmonary perfusion and inhalative carbon monoxide inhibits CPB-mediated pulmonary inflammation as well as pulmonary apoptosis stronger than pulmonary perfusion or carbon monoxide alone.

Key Words: Cardiopulmonary bypass • Inflammation • Pulmonary perfusion • Carbon monoxide

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				U. Goebel and M. Siepe eComment: Carbon monoxide and its vasodilatative properties: another good reason for clinical implication Interactive CardioVascular and Thoracic Surgery, December 1, 2008; 7(6): 962 - 963. [Full Text] [PDF]