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Does the antisecretory peptide AF-16 reduce lung oedema in experimental ARDS?
Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Surgical Sciences, Hedenstierna laboratory.
Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Surgical Sciences, Hedenstierna laboratory. Anthea Hosp, GVM Care & Res, Cardiac Anesthesia & Intens Care, Bari, Italy.
Univ Gothenburg, Inst Biomed, Gothenburg, Sweden.
Natl Vet Inst, Dept Pathol & Wildlife Dis, Uppsala, Sweden.
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(English)In: Upsala Journal of Medical Sciences, ISSN 0300-9734, E-ISSN 2000-1967Article in journal (Refereed) Epub ahead of print
Abstract [en]

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.

Place, publisher, year, edition, pages
TAYLOR & FRANCIS LTD.
Keywords [en]
AF-16 antisecretory factor, ARDS, extravascular lung water, pulmonary oedema
National Category
Anesthesiology and Intensive Care
Identifiers
URN: urn:nbn:se:uu:diva-397601DOI: 10.1080/03009734.2019.1685029ISI: 000495161000001PubMedID: 31701794OAI: oai:DiVA.org:uu-397601DiVA, id: diva2:1372217
Funder
Swedish Heart Lung Foundation, 20170531Swedish Research Council, X2015-99x-22731-01-4Available from: 2019-11-22 Created: 2019-11-22 Last updated: 2019-11-22

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Barrueta Tenhunen, AnnelieMassaro, FabriziaLarsson, AndersLarsson, AndersPerchiazzi, Gaetano
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