Abstract
Background: Acute respiratory distress syndrome (ARDS) is an acute inflammatory condition with pulmonary capillary leakage and lung oedema formation. There is currently no pharmacologic treatment for the condition. The antisecretory peptide AF-16 reduces oedema in experimental traumatic brain injury. In this study, we tested AF-16 in an experimental porcine model of ARDS.Methods: Under surgical anaesthesia 12 piglets were subjected to lung lavage followed by 2 hours of injurious ventilation. Every hour for 4 hours, measurements of extravascular lung water (EVLW), mechanics of the respiratory system, and hemodynamics were obtained.Results: There was a statistically significant (p = 0.006, two-way ANOVA) reduction of EVLW in the AF-16 group compared with controls. However, this was not mirrored in any improvement in the wet-to-dry ratio of lung tissue samples, histology, inflammatory markers, lung mechanics, or gas exchange.Conclusions: This pilot study suggests that AF-16 might improve oedema resolution as indicated by a reduction in EVLW in experimental ARDS.
Highlights
Acute respiratory distress syndrome (ARDS) is an inflammatory lung injury with acute onset, characterized by increased pulmonary vascular permeability, pulmonary oedema, increased lung weight, and loss of aerated lung tissue (1)
Fluid administration was standardized according to the protocol, and both groups maintained an adequate diuresis throughout the experiment. This pilot study in experimental ARDS suggests that the antisecretory peptide Antisecretory factor (AF)-16 might improve oedema resolution, indicated by a decrease in extravascular lung water (EVLW)
We used a two-hit model for ARDS, consisting of lung lavage followed by injurious ventilation
Summary
Acute respiratory distress syndrome (ARDS) is an inflammatory lung injury with acute onset, characterized by increased pulmonary vascular permeability, pulmonary oedema, increased lung weight, and loss of aerated lung tissue (1). In clinical trials increased concentrations of AF in plasma is associated with a decrease of symptoms in different conditions such as inflammatory bowel disease, gastroenteritis, and Meniere’s disease (19–21) It is unknown whether AF or AF-16 has any effect on oedema resolution in the lungs. We hypothesised that the peptide AF-16 could reduce pulmonary oedema formation in a porcine model of ARDS by altering the quantity of extravascular lung water (EVLW), the inflammatory response, and the pressure–volume (PV) relation of the lung. Results: There was a statistically significant (p 1⁄4 0.006, two-way ANOVA) reduction of EVLW in the AF16 group compared with controls This was not mirrored in any improvement in the wet-todry ratio of lung tissue samples, histology, inflammatory markers, lung mechanics, or gas exchange. Conclusions: This pilot study suggests that AF-16 might improve oedema resolution as indicated by a reduction in EVLW in experimental ARDS
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