Surfactant reduces extravascular lung water and invasion of polymorphonuclear leukocytes into the lung in a piglet model of airway lavage

Acute respiratory distress syndrome (ARDS) in newborns and young infants is linked with an inflammatory response of the lungs which affects the capillary-alveolar permeability, epithelial integrity and type I and II pneumocyte function. Abundant extravascular lung water with a high protein content i...

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Veröffentlicht in:Pulmonary pharmacology & therapeutics 2005-04, Vol.18 (2), p.129-139
Hauptverfasser: Krause, Martin F., Wiemann, Tina, Reisner, Anja, Orlowska-Volk, Marzenna, Köhler, Heike, Ankermann, Tobias
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Sprache:eng
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Zusammenfassung:Acute respiratory distress syndrome (ARDS) in newborns and young infants is linked with an inflammatory response of the lungs which affects the capillary-alveolar permeability, epithelial integrity and type I and II pneumocyte function. Abundant extravascular lung water with a high protein content inactivates surfactant together with the enzymatic action of polymorphonuclear leukocytes (PMNL). We asked if a decrease in extravascular lung water and a reduction in lung infiltration with PMNL could be achieved by surfactant administration (Curosurf®) within 6h of mechanical ventilation when given in a newborn piglet model of repeated airway lavage. Improvements in gas exchange and lung mechanics were predominantly caused by resorption of extravascular lung water rather than by the reopening of alveolar atelectases. PMNL were significantly reduced in the bronchoalveolar lavage fluid after 6h of mechanical ventilation. However, acute phase cytokines (IL-6, TNF-α) remained unchanged, except for IL-8 which increased after administration of surfactant. We conclude that the decrease in extravascular lung water and in infiltration with PMNL following surfactant administration is accomplished within 6h through mechanisms different from attenuation of pro-inflammatory cytokines. Surfactant treatment for newborn and infant ARDS might therefore improve fluid overload and atelectasis and reduce PMNL infiltration.
ISSN:1094-5539
1522-9629
DOI:10.1016/j.pupt.2004.11.003