Name of journal: Journal of burn care & research : official publication of the American Burn AssociationAbstract: Inhalation injury is a significant cause of morbidity and mortality in the burn patient population. However, the pathogenesis of inhalation injury and its potential involvement in burn shock is not well understood. Pre-clinical studies have shown endothelial injury, as measured by syndecan-1 (SDC-1) levels, to be involved in the increased vascular permeability seen in shock states. Furthermore, the lung has been identified as a site of significant SDC-1 shedding. Here we aim to characterize the contribution of endotheliopathy caused by inhalation alone in a swine model. When comparing injured animals, the fold-change of circulating SDC-1 levels from pre-injury was significantly higher at hour 2, 4 and 6 post-injury (p=.0045, p=.0017 and p<.001, respectively). When comparing control animals, the fold change of SDC-1 from pre-injury was not significant at any timepoint. When comparing injured animals vs. controls, the fold change of SDC-1 injured animals was significantly greater at hours 2, 4, 6 and 18 (p=.004, p=.03, p<.001 and p=.03, respectively). Histological sections showed higher lung injury severity compared to control uninjured lungs (0.56 vs 0.38, p<0.001). This novel animal model shows significant increases in SDC-1 levels that provide evidence for the connection between smoke inhalation injury and endothelial injury. Further understanding of the mechanisms underlying inhalation injury and its contribution to shock physiology may aid in development of early, more targeted therapies. Copyright © The Author(s) 2023. Published by Oxford University Press on behalf of the American Burn Association. All rights reserved. For permissions, please e-mail: [email protected].All authors: Kelly EJ, Carney BC, Oliver MA, Keyloun JW, Prindeze NJ, Nisar S, Moffatt LT, Shupp JWFiscal year: FY2023 Digital Object Identifier:

https://dx.doi.org/10.1093/jbcr/irad018

Date added to catalog: 2023-04-11

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Item type	Current library	Collection	Call number	Status	Date due	Barcode
Journal Article	MedStar Authors Catalog	Article		Available

Available online through MWHC library: 2006 - present, Available in print through MWHC library: 2006 - present

Inhalation injury is a significant cause of morbidity and mortality in the burn patient population. However, the pathogenesis of inhalation injury and its potential involvement in burn shock is not well understood. Pre-clinical studies have shown endothelial injury, as measured by syndecan-1 (SDC-1) levels, to be involved in the increased vascular permeability seen in shock states. Furthermore, the lung has been identified as a site of significant SDC-1 shedding. Here we aim to characterize the contribution of endotheliopathy caused by inhalation alone in a swine model. When comparing injured animals, the fold-change of circulating SDC-1 levels from pre-injury was significantly higher at hour 2, 4 and 6 post-injury (p=.0045, p=.0017 and p<.001, respectively). When comparing control animals, the fold change of SDC-1 from pre-injury was not significant at any timepoint. When comparing injured animals vs. controls, the fold change of SDC-1 injured animals was significantly greater at hours 2, 4, 6 and 18 (p=.004, p=.03, p<.001 and p=.03, respectively). Histological sections showed higher lung injury severity compared to control uninjured lungs (0.56 vs 0.38, p<0.001). This novel animal model shows significant increases in SDC-1 levels that provide evidence for the connection between smoke inhalation injury and endothelial injury. Further understanding of the mechanisms underlying inhalation injury and its contribution to shock physiology may aid in development of early, more targeted therapies. Copyright © The Author(s) 2023. Published by Oxford University Press on behalf of the American Burn Association. All rights reserved. For permissions, please e-mail: [email protected].

English