Fresh Frozen Plasma Lessens Pulmonary Endothelial Inflammation and Hyperpermeability After Hemorrhagic Shock and Is Associated With Loss of Syndecan 1
- 1 September 2013
- journal article
- basic science-aspects
- Published by Ovid Technologies (Wolters Kluwer Health) in Shock
- Vol. 40 (3), 195-202
- https://doi.org/10.1097/shk.0b013e31829f91fc
Abstract
We have recently demonstrated that injured patients in hemorrhagic shock shed syndecan 1 and that the early use of fresh frozen plasma (FFP) in these patients is correlated with improved clinical outcomes. As the lungs are frequently injured after trauma, we hypothesized that hemorrhagic shock–induced shedding of syndecan 1 exposes the underlying pulmonary vascular endothelium to injury resulting in inflammation and hyperpermeability and that these effects would be mitigated by FFP. In vitro, pulmonary endothelial permeability, endothelial monolayer flux, transendothelial electrical resistance, and leukocyte-endothelial binding were measured in pulmonary endothelial cells after incubation with equal volumes of FFP or lactated Ringer’s (LR). In vivo, using a coagulopathic mouse model of trauma and hemorrhagic shock, pulmonary hyperpermeability, neutrophil infiltration, and syndecan 1 expression and systemic shedding were assessed after 3 h of resuscitation with either 1× FFP or 3× LR and compared with shock alone and shams. In vitro, endothelial permeability and flux were decreased, transendothelial electrical resistance was increased, and leukocyte-endothelial binding was inhibited by FFP compared with LR-treated endothelial cells. In vivo, hemorrhagic shock was associated with systemic shedding of syndecan 1, which correlated with decreased pulmonary syndecan 1 and increased pulmonary vascular hyperpermeability and inflammation. Fresh frozen plasma resuscitation, compared with LR resuscitation, abrogated these injurious effects. After hemorrhagic shock, FFP resuscitation inhibits endothelial cell hyperpermeability and inflammation and restores pulmonary syndecan 1 expression. Modulation of pulmonary syndecan 1 expression may mechanistically contribute to the beneficial effects FFP.Keywords
This publication has 36 references indexed in Scilit:
- Traumatic Brain Injury and Hemorrhagic ShockShock, 2012
- Molecular functions of syndecan-1 in diseaseMatrix Biology, 2012
- Modulation of Syndecan-1 Shedding after Hemorrhagic Shock and ResuscitationPLOS ONE, 2011
- Real-time label-free monitoring of adipose-derived stem cell differentiation with electric cell-substrate impedance sensingProceedings of the National Academy of Sciences of the United States of America, 2011
- Quantitative Assessment of Intestinal Injury Using a Novel In Vivo, Near-Infrared Imaging TechniqueMolecular Imaging, 2010
- Antithrombin reduces shedding of the endothelial glycocalyx following ischaemia/reperfusionCardiovascular Research, 2009
- Staphylococcus aureus Beta-Toxin Induces Lung Injury through Syndecan-1The American Journal of Pathology, 2009
- Increased Plasma and Platelet to Red Blood Cell Ratios Improves Outcome in 466 Massively Transfused Civilian Trauma PatientsAnnals of Surgery, 2008
- Shedding of the Endothelial Glycocalyx in Patients Undergoing Major Vascular Surgery With Global and Regional IschemiaCirculation, 2007
- Electrical method for detection of endothelial cell shape change in real time: assessment of endothelial barrier function.Proceedings of the National Academy of Sciences of the United States of America, 1992