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Selenium prevents microparticle-induced endothelial inflammation in patients after cardiopulmonary resuscitation
INTRODUCTION: Microparticles are elevated in patients after successful cardiopulmonary resuscitation (CPR) and may play a role in the development of endothelial dysfunction seen in post-cardiac arrest syndrome (PCAS), a life threatening disease with high mortality. To identify mechanisms of endothel...
Autores principales: | , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
BioMed Central
2015
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4367830/ https://www.ncbi.nlm.nih.gov/pubmed/25886988 http://dx.doi.org/10.1186/s13054-015-0774-3 |
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author | Fink, Katrin Moebes, Monica Vetter, Caroline Bourgeois, Natascha Schmid, Bonaventura Bode, Christoph Helbing, Thomas Busch, Hans-Jörg |
author_facet | Fink, Katrin Moebes, Monica Vetter, Caroline Bourgeois, Natascha Schmid, Bonaventura Bode, Christoph Helbing, Thomas Busch, Hans-Jörg |
author_sort | Fink, Katrin |
collection | PubMed |
description | INTRODUCTION: Microparticles are elevated in patients after successful cardiopulmonary resuscitation (CPR) and may play a role in the development of endothelial dysfunction seen in post-cardiac arrest syndrome (PCAS), a life threatening disease with high mortality. To identify mechanisms of endothelial activation and to develop novel approaches in the therapy of PCAS, the impact of selenium, a trace element with antioxidative properties, was characterized in endothelial dysfunction induced by microparticles of resuscitated patients. Additionally, course of plasma selenium levels was characterized in the first 72 hours post-CPR. METHODS: Endothelial cells were exposed to microparticles isolated of the peripheral blood of resuscitated patients, and leukocyte-endothelial interaction was measured by dynamic adhesion assay. Expression of adhesion molecules was assessed by immunoblotting and flow chamber. Blood samples were drawn 24, 48 and 72 hours after CPR for determination of plasma selenium levels in 77 resuscitated patients; these were compared to 50 healthy subjects and 50 patients with stable cardiac disease and correlated with severity of illness and outcome. RESULTS: Microparticles of resuscitated patients enhance monocyte-endothelial interaction by up-regulation of ICAM-1 and VCAM-1. Selenium administration diminished ICAM-1 and VCAM-1-mediated monocyte adhesion induced by microparticles of resuscitated patients, suggesting that selenium has anti-inflammatory effects after CPR. Lowered selenium plasma levels were observed in resuscitated patients compared to controls and selenium levels immediately and 24 hours after CPR, inversely correlated with clinical course and outcome after resuscitation. CONCLUSIONS: Endothelial dysfunction is a pivotal feature of PCAS and is partly driven by microparticles of resuscitated patients. Administration of selenium exerted anti-inflammatory effects and prevented microparticle-mediated endothelial dysfunction. Decline of selenium was observed in plasma of patients after CPR and is a novel predictive marker of ICU mortality, suggesting selenium consumption promotes inflammation in PCAS. ELECTRONIC SUPPLEMENTARY MATERIAL: The online version of this article (doi:10.1186/s13054-015-0774-3) contains supplementary material, which is available to authorized users. |
format | Online Article Text |
id | pubmed-4367830 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2015 |
publisher | BioMed Central |
record_format | MEDLINE/PubMed |
spelling | pubmed-43678302015-03-21 Selenium prevents microparticle-induced endothelial inflammation in patients after cardiopulmonary resuscitation Fink, Katrin Moebes, Monica Vetter, Caroline Bourgeois, Natascha Schmid, Bonaventura Bode, Christoph Helbing, Thomas Busch, Hans-Jörg Crit Care Research INTRODUCTION: Microparticles are elevated in patients after successful cardiopulmonary resuscitation (CPR) and may play a role in the development of endothelial dysfunction seen in post-cardiac arrest syndrome (PCAS), a life threatening disease with high mortality. To identify mechanisms of endothelial activation and to develop novel approaches in the therapy of PCAS, the impact of selenium, a trace element with antioxidative properties, was characterized in endothelial dysfunction induced by microparticles of resuscitated patients. Additionally, course of plasma selenium levels was characterized in the first 72 hours post-CPR. METHODS: Endothelial cells were exposed to microparticles isolated of the peripheral blood of resuscitated patients, and leukocyte-endothelial interaction was measured by dynamic adhesion assay. Expression of adhesion molecules was assessed by immunoblotting and flow chamber. Blood samples were drawn 24, 48 and 72 hours after CPR for determination of plasma selenium levels in 77 resuscitated patients; these were compared to 50 healthy subjects and 50 patients with stable cardiac disease and correlated with severity of illness and outcome. RESULTS: Microparticles of resuscitated patients enhance monocyte-endothelial interaction by up-regulation of ICAM-1 and VCAM-1. Selenium administration diminished ICAM-1 and VCAM-1-mediated monocyte adhesion induced by microparticles of resuscitated patients, suggesting that selenium has anti-inflammatory effects after CPR. Lowered selenium plasma levels were observed in resuscitated patients compared to controls and selenium levels immediately and 24 hours after CPR, inversely correlated with clinical course and outcome after resuscitation. CONCLUSIONS: Endothelial dysfunction is a pivotal feature of PCAS and is partly driven by microparticles of resuscitated patients. Administration of selenium exerted anti-inflammatory effects and prevented microparticle-mediated endothelial dysfunction. Decline of selenium was observed in plasma of patients after CPR and is a novel predictive marker of ICU mortality, suggesting selenium consumption promotes inflammation in PCAS. ELECTRONIC SUPPLEMENTARY MATERIAL: The online version of this article (doi:10.1186/s13054-015-0774-3) contains supplementary material, which is available to authorized users. BioMed Central 2015-02-26 2015 /pmc/articles/PMC4367830/ /pubmed/25886988 http://dx.doi.org/10.1186/s13054-015-0774-3 Text en © Fink et al.; licensee BioMed Central. 2015 This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly credited. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated. |
spellingShingle | Research Fink, Katrin Moebes, Monica Vetter, Caroline Bourgeois, Natascha Schmid, Bonaventura Bode, Christoph Helbing, Thomas Busch, Hans-Jörg Selenium prevents microparticle-induced endothelial inflammation in patients after cardiopulmonary resuscitation |
title | Selenium prevents microparticle-induced endothelial inflammation in patients after cardiopulmonary resuscitation |
title_full | Selenium prevents microparticle-induced endothelial inflammation in patients after cardiopulmonary resuscitation |
title_fullStr | Selenium prevents microparticle-induced endothelial inflammation in patients after cardiopulmonary resuscitation |
title_full_unstemmed | Selenium prevents microparticle-induced endothelial inflammation in patients after cardiopulmonary resuscitation |
title_short | Selenium prevents microparticle-induced endothelial inflammation in patients after cardiopulmonary resuscitation |
title_sort | selenium prevents microparticle-induced endothelial inflammation in patients after cardiopulmonary resuscitation |
topic | Research |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4367830/ https://www.ncbi.nlm.nih.gov/pubmed/25886988 http://dx.doi.org/10.1186/s13054-015-0774-3 |
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