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The impact of mechanical ventilation on the systemic inflammatory response of patients with severe acute exacerbation of COPD

Georgios Hillas, Paraskevi Katsaounou, Fotis Perlikos, Dimitris Toumpanakis, Eleni Litsiou, Sofia Nikolakopoulou, Kostas Sagris, Theodoros Vassilakopoulos
European Respiratory Journal 2014 44: 1388; DOI:
Georgios Hillas
1Department of Critical Care and Pulmonary Services, University of Athens Medical School, Evangelismos Hospital, Athens, Greece
2Department of Respiratory and Critical Care Medicine, Research Unit, ”Sotiria" Chest Diseases Hospital, Athens, Greece
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Paraskevi Katsaounou
1Department of Critical Care and Pulmonary Services, University of Athens Medical School, Evangelismos Hospital, Athens, Greece
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Fotis Perlikos
1Department of Critical Care and Pulmonary Services, University of Athens Medical School, Evangelismos Hospital, Athens, Greece
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Dimitris Toumpanakis
1Department of Critical Care and Pulmonary Services, University of Athens Medical School, Evangelismos Hospital, Athens, Greece
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Eleni Litsiou
1Department of Critical Care and Pulmonary Services, University of Athens Medical School, Evangelismos Hospital, Athens, Greece
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Sofia Nikolakopoulou
2Department of Respiratory and Critical Care Medicine, Research Unit, ”Sotiria" Chest Diseases Hospital, Athens, Greece
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Kostas Sagris
2Department of Respiratory and Critical Care Medicine, Research Unit, ”Sotiria" Chest Diseases Hospital, Athens, Greece
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Theodoros Vassilakopoulos
1Department of Critical Care and Pulmonary Services, University of Athens Medical School, Evangelismos Hospital, Athens, Greece
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Abstract

Introduction: Resistive breathing due to airflow limitation is observed during the natural course of chronic obstructive pulmonary disease (COPD), especially during acute exacerbation of COPD (AECOPD) and is characterized by elevated cytokine plasma levels.

Objective: To test the hypothesis that the respiratory muscles and/or the mechanically stressed lung contribute to the elevated cytokine plasma levels in patients with AECOPD and that these levels would be decreased after respiratory muscles relaxation due to mechanical ventilation.

Methods: 30 patients with AECOPD, that led to endotracheal intubation and mechanical ventilation (intervention group) and 7 patients with COPD in steady state, which were intubated and mechanically ventilated for elective surgery (control group) were used.

Blood samples were collected just before, 20 minutes and 6 hours after intubation (intervention group) and just before and 20 minutes after intubation (control group).

Luminex 100 IS technique was used to access the cytokine plasma levels.

Results: IL-6, IL-8, Eotaxin and EGF plasma levels decreased statistically significantly over time, whereas IL-5, IL-8, TNF-α, INF-γ, MCP-1 and RANTES levels didn't change significantly over time (intervention group).

Plasma levels of all measured cytokines did not change significantly over time in the control group.

Conclusions: Application of mechanical ventilation in patients with AECOPD leads to decreased plasma levels for circulating IL-6, IL-10, Eotaxin and EGF. The respiratory muscles and especially the contracting diaphragm and/or the mechanically stressed "inflammatory" lung could contribute to the elevate levels of these cytokines.

  • COPD - exacerbations
  • Mechanical ventilation - interactions and complications
  • Inflammation
  • © 2014 ERS
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The impact of mechanical ventilation on the systemic inflammatory response of patients with severe acute exacerbation of COPD
Georgios Hillas, Paraskevi Katsaounou, Fotis Perlikos, Dimitris Toumpanakis, Eleni Litsiou, Sofia Nikolakopoulou, Kostas Sagris, Theodoros Vassilakopoulos
European Respiratory Journal Sep 2014, 44 (Suppl 58) 1388;

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The impact of mechanical ventilation on the systemic inflammatory response of patients with severe acute exacerbation of COPD
Georgios Hillas, Paraskevi Katsaounou, Fotis Perlikos, Dimitris Toumpanakis, Eleni Litsiou, Sofia Nikolakopoulou, Kostas Sagris, Theodoros Vassilakopoulos
European Respiratory Journal Sep 2014, 44 (Suppl 58) 1388;
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