Document Detail


Reduced pulmonary inflammatory response during cardiopulmonary bypass: effects of combined pulmonary perfusion and carbon monoxide inhalation.
MedLine Citation:
PMID:  18829339     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
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-alpha, 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-alpha (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-kappaB 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.
Authors:
Ulrich Goebel; Matthias Siepe; Anne Mecklenburg; Torsten Doenst; Friedhelm Beyersdorf; Torsten Loop; Christian Schlensak
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Publication Detail:
Type:  Comparative Study; Journal Article; Research Support, Non-U.S. Gov't     Date:  2008-10-01
Journal Detail:
Title:  European journal of cardio-thoracic surgery : official journal of the European Association for Cardio-thoracic Surgery     Volume:  34     ISSN:  1873-734X     ISO Abbreviation:  Eur J Cardiothorac Surg     Publication Date:  2008 Dec 
Date Detail:
Created Date:  2008-11-21     Completed Date:  2009-03-05     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  8804069     Medline TA:  Eur J Cardiothorac Surg     Country:  Germany    
Other Details:
Languages:  eng     Pagination:  1165-72     Citation Subset:  IM    
Affiliation:
Department of Anesthesiology and Critical Care Medicine, University Medical Center Freiburg, Freiburg, Germany.
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MeSH Terms
Descriptor/Qualifier:
Administration, Inhalation
Animals
Apoptosis
Biological Markers / analysis
Carbon Monoxide / administration & dosage*
Cardiopulmonary Bypass / adverse effects*
Caspase 3 / analysis
Electrophoretic Mobility Shift Assay
Enzyme-Linked Immunosorbent Assay
Interleukin-10 / analysis
Interleukin-6 / analysis
Lung / immunology,  pathology
Models, Animal
NF-kappa B / analysis
Perfusion
Pneumonia / etiology*,  pathology,  therapy*
Protein Binding
Random Allocation
Swine
Transcription Factor AP-1 / analysis
Tumor Necrosis Factor-alpha / analysis
Chemical
Reg. No./Substance:
0/Biological Markers; 0/Interleukin-6; 0/NF-kappa B; 0/Transcription Factor AP-1; 0/Tumor Necrosis Factor-alpha; 130068-27-8/Interleukin-10; 630-08-0/Carbon Monoxide; EC 3.4.22.-/Caspase 3

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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