Effects of Positive End-Expiratory Pressure and Spontaneous Breathing Activity on Regional Lung Inflammation in Experimental Acute Respiratory Distress Syndrome
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- Thomas Kiss
- Pulmonary Engineering Group, Department of Anesthesiology and Intensive Care Medicine, University Hospital Carl Gustav Carus, Technische Universität Dresden, Dresden, Germany.
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- Thomas Bluth
- Pulmonary Engineering Group, Department of Anesthesiology and Intensive Care Medicine, University Hospital Carl Gustav Carus, Technische Universität Dresden, Dresden, Germany.
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- Anja Braune
- Pulmonary Engineering Group, Department of Anesthesiology and Intensive Care Medicine, University Hospital Carl Gustav Carus, Technische Universität Dresden, Dresden, Germany.
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- Robert Huhle
- Pulmonary Engineering Group, Department of Anesthesiology and Intensive Care Medicine, University Hospital Carl Gustav Carus, Technische Universität Dresden, Dresden, Germany.
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- Axel Denz
- Department of Surgery, Friedrich-Alexander-Universität Erlangen-Nürnberg, Erlangen, Germany.
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- Moritz Herzog
- Pulmonary Engineering Group, Department of Anesthesiology and Intensive Care Medicine, University Hospital Carl Gustav Carus, Technische Universität Dresden, Dresden, Germany.
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- Johannes Herold
- Pulmonary Engineering Group, Department of Anesthesiology and Intensive Care Medicine, University Hospital Carl Gustav Carus, Technische Universität Dresden, Dresden, Germany.
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- Luigi Vivona
- Pulmonary Engineering Group, Department of Anesthesiology and Intensive Care Medicine, University Hospital Carl Gustav Carus, Technische Universität Dresden, Dresden, Germany.
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- Marco Millone
- Pulmonary Engineering Group, Department of Anesthesiology and Intensive Care Medicine, University Hospital Carl Gustav Carus, Technische Universität Dresden, Dresden, Germany.
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- Alice Bergamaschi
- Pulmonary Engineering Group, Department of Anesthesiology and Intensive Care Medicine, University Hospital Carl Gustav Carus, Technische Universität Dresden, Dresden, Germany.
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- Michael Andreeff
- Institute of Nuclear Medicine, University Hospital Carl Gustav Carus, Dresden, Germany.
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- Martin Scharffenberg
- Pulmonary Engineering Group, Department of Anesthesiology and Intensive Care Medicine, University Hospital Carl Gustav Carus, Technische Universität Dresden, Dresden, Germany.
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- Jakob Wittenstein
- Pulmonary Engineering Group, Department of Anesthesiology and Intensive Care Medicine, University Hospital Carl Gustav Carus, Technische Universität Dresden, Dresden, Germany.
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- Marcos F. Vidal Melo
- Department of Anesthesia, Critical Care and Pain Medicine, Massachusetts General Hospital, Harvard University, Boston, MA.
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- Thea Koch
- Pulmonary Engineering Group, Department of Anesthesiology and Intensive Care Medicine, University Hospital Carl Gustav Carus, Technische Universität Dresden, Dresden, Germany.
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- Patricia R. M. Rocco
- Laboratory of Pulmonary Investigation, Carlos Chagas Filho Institute of Biophysics, Federal University of Rio de Janeiro, Rio de Janeiro, Brazil.
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- Paolo Pelosi
- Department of Surgical Sciences and Integrated Diagnostics, Policlinico San Martino Hospital, IRCCS for Oncology, University of Genoa, Genoa, Italy.
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- Jörg Kotzerke
- Institute of Nuclear Medicine, University Hospital Carl Gustav Carus, Dresden, Germany.
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- Marcelo Gama de Abreu
- Pulmonary Engineering Group, Department of Anesthesiology and Intensive Care Medicine, University Hospital Carl Gustav Carus, Technische Universität Dresden, Dresden, Germany.
Description
<jats:sec> <jats:title>Objectives:</jats:title> <jats:p>To determine the impact of positive end-expiratory pressure during mechanical ventilation with and without spontaneous breathing activity on regional lung inflammation in experimental nonsevere acute respiratory distress syndrome.</jats:p> </jats:sec> <jats:sec> <jats:title>Design:</jats:title> <jats:p>Laboratory investigation.</jats:p> </jats:sec> <jats:sec> <jats:title>Setting:</jats:title> <jats:p>University hospital research facility.</jats:p> </jats:sec> <jats:sec> <jats:title>Subjects:</jats:title> <jats:p>Twenty-four pigs (28.1–58.2 kg).</jats:p> </jats:sec> <jats:sec> <jats:title>Interventions:</jats:title> <jats:p>In anesthetized animals, intrapleural pressure sensors were placed thoracoscopically in ventral, dorsal, and caudal regions of the left hemithorax. Lung injury was induced with saline lung lavage followed by injurious ventilation in supine position. During airway pressure release ventilation with low tidal volumes, positive end-expiratory pressure was set 4 cm H<jats:sub>2</jats:sub>O above the level to reach a positive transpulmonary pressure in caudal regions at end-expiration (best-positive end-expiratory pressure). Animals were randomly assigned to one of four groups (<jats:italic toggle="yes">n</jats:italic> = 6/group; 12 hr): 1) no spontaneous breathing activity and positive end-expiratory pressure = best-positive end-expiratory pressure – 4 cm H<jats:sub>2</jats:sub>O, 2) no spontaneous breathing activity and positive end-expiratory pressure = best-positive end-expiratory pressure + 4 cm H<jats:sub>2</jats:sub>O, 3) spontaneous breathing activity and positive end-expiratory pressure = best-positive end-expiratory pressure + 4 cm H<jats:sub>2</jats:sub>O, 4) spontaneous breathing activity and positive end-expiratory pressure = best-positive end-expiratory pressure – 4 cm H<jats:sub>2</jats:sub>O.</jats:p> </jats:sec> <jats:sec> <jats:title>Measurements and Main Results:</jats:title> <jats:p>Global lung inflammation assessed by specific [<jats:sup>18</jats:sup>F]fluorodeoxyglucose uptake rate (median [25–75% percentiles], min<jats:sup>–1</jats:sup>) was decreased with higher compared with lower positive end-expiratory pressure both without spontaneous breathing activity (0.029 [0.027–0.030] vs 0.044 [0.041–0.065]; <jats:italic toggle="yes">p</jats:italic> = 0.004) and with spontaneous breathing activity (0.032 [0.028–0.043] vs 0.057 [0.042–0.075]; <jats:italic toggle="yes">p</jats:italic> = 0.016). Spontaneous breathing activity did not increase global lung inflammation. Lung inflammation in dorsal regions correlated with transpulmonary driving pressure from spontaneous breathing at lower (<jats:italic toggle="yes">r</jats:italic> = 0.850; <jats:italic toggle="yes">p</jats:italic> = 0.032) but not higher positive end-expiratory pressure (<jats:italic toggle="yes">r</jats:italic> = 0.018; <jats:italic toggle="yes">p</jats:italic> = 0.972). Higher positive end-expiratory pressure resulted in a more homogeneous distribution of aeration and regional transpulmonary pressures at end-expiration along the ventral-dorsal gradient, as well as a shift of the perfusion center toward dependent zones in the presence of spontaneous breathing activity.</jats:p> </jats:sec> <jats:sec> <jats:title>Conclusions:</jats:title> <jats:p>In experimental mild-to-moderate acute respiratory distress syndrome, positive end-expiratory pressure levels that stabilize dependent lung regions reduce global lung inflammation during mechanical ventilation, independent from spontaneous breathing activity.</jats:p> </jats:sec>
Journal
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- Critical Care Medicine
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Critical Care Medicine 47 (4), e358-e365, 2019-04
Ovid Technologies (Wolters Kluwer Health)
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Details 詳細情報について
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- CRID
- 1361418518564384512
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- ISSN
- 00903493
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- Data Source
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- Crossref