Extracorporeal Membrane Oxygenation Causes Loss of Intestinal Epithelial Barrier in the Newborn Piglet
| Autor: | R Britt McILwain, John P. Clancy, Dongning He, Ashish Kurundkar, Rajendra Karnatak, Gattadahalli M. Anantharamaiah, Joseph G Timpa, Cheryl R. Killingsworth, Yolanda E. Hartman, Mary Lauren Neel, Akhil Maheshwari |
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| Rok vydání: | 2010 |
| Předmět: |
Lipopolysaccharides
Cell Membrane Permeability Lipopolysaccharide Swine medicine.medical_treatment Gene Expression Inflammation Biology Article Tight Junctions Andrology chemistry.chemical_compound Extracorporeal Membrane Oxygenation Myosin medicine Extracorporeal membrane oxygenation Animals Humans Intestinal Mucosa Child Cytoskeleton Barrier function Bacteria Infant Newborn Epithelium Gut Epithelium surgical procedures operative medicine.anatomical_structure Animals Newborn Intestinal Absorption chemistry Pediatrics Perinatology and Child Health Immunology medicine.symptom |
| Zdroj: | Pediatric Research. 68:128-133 |
| ISSN: | 1530-0447 0031-3998 |
| DOI: | 10.1203/pdr.0b013e3181e4c9f8 |
| Popis: | Extracorporeal membrane oxygenation (ECMO) is an important life-support system used in neonates and young children with intractable cardiorespiratory failure. In this study, we used our porcine neonatal model of venoarterial ECMO to investigate whether ECMO causes gut barrier dysfunction. We subjected 3-week-old previously-healthy piglets to venoarterial ECMO for up to 8 hours and evaluated gut mucosal permeability, bacterial translocation, plasma levels of bacterial products, and ultrastructural changes in gut epithelium. We also measured plasma lipopolysaccharide (LPS) levels in a small cohort of human neonates receiving ECMO. In our porcine model, ECMO caused a rapid increase in gut mucosal permeability within the first 2 hours of treatment, leading to a 6–10 fold rise in circulating bacterial products. These changes in barrier function were associated with cytoskeletal condensation in epithelial cells, which was explained by phosphorylation of a myosin II regulatory light chain. In support of these findings, we also detected elevated plasma LPS levels in human neonates receiving ECMO, indicating a similar loss of gut barrier function in these infants. Based on these data, we conclude that ECMO is an independent cause of gut barrier dysfunction, and that bacterial translocation may be an important contributor to ECMO-related inflammation. |
| Databáze: | OpenAIRE |
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