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Investigation of the pathophysiology of cardiopulmonary bypass using rodent extracorporeal life support model

BACKGROUND: Extracorporeal life support (ECLS) systems are life-saving devices used for treating patients with severe cardiopulmonary failure. In this study, we implemented a rat model of ECLS without the administration of inotropes or vasopressors. METHODS: The rats underwent 5 min of untreated asp...

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Autores principales: Chang, Ru-Wen, Luo, Chien-Ming, Yu, Hsi-Yu, Chen, Yih-Sharng, Wang, Chih-Hsien
Formato: Online Artículo Texto
Lenguaje:English
Publicado: BioMed Central 2017
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5433070/
https://www.ncbi.nlm.nih.gov/pubmed/28506218
http://dx.doi.org/10.1186/s12872-017-0558-6
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author Chang, Ru-Wen
Luo, Chien-Ming
Yu, Hsi-Yu
Chen, Yih-Sharng
Wang, Chih-Hsien
author_facet Chang, Ru-Wen
Luo, Chien-Ming
Yu, Hsi-Yu
Chen, Yih-Sharng
Wang, Chih-Hsien
author_sort Chang, Ru-Wen
collection PubMed
description BACKGROUND: Extracorporeal life support (ECLS) systems are life-saving devices used for treating patients with severe cardiopulmonary failure. In this study, we implemented a rat model of ECLS without the administration of inotropes or vasopressors. METHODS: The rats underwent 5 min of untreated asphyxial cardiac arrest and were resuscitated by ECLS for 30 min. The right external jugular vein and right femoral artery were separately cannulated to the ECLS outflow and inflow, respectively. Thereafter, ECLS was terminated, wounds were closed, and mechanical ventilation was provided for another 90 min. Subsequently, blood gas and hemodynamic analyses were performed. The plasma levels of C-reactive protein (CRP), interleukin (IL)-6, IL-10, and tumor necrosis factor-alpha (TNF-α) were measured 120 min after reperfusion. RESULTS: The metabolic rate of lactate in the group of asphyxial cardiac arrest rescued by ECLS was slow; therefore, the pH at 120 min after reperfusion was significantly lower in this group than that in the group of normal rats treated with ECLS. The hemodynamic data showed no between-group differences. The plasma levels of CRP, IL-6, IL-10, and TNF-α increased after ECLS treatment. CONCLUSIONS: We successfully established a rodent ECLS model, which might be a useful approach for studying the pathophysiology induced by ECLS under clinical conditions. ELECTRONIC SUPPLEMENTARY MATERIAL: The online version of this article (doi:10.1186/s12872-017-0558-6) contains supplementary material, which is available to authorized users.
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spelling pubmed-54330702017-05-17 Investigation of the pathophysiology of cardiopulmonary bypass using rodent extracorporeal life support model Chang, Ru-Wen Luo, Chien-Ming Yu, Hsi-Yu Chen, Yih-Sharng Wang, Chih-Hsien BMC Cardiovasc Disord Research Article BACKGROUND: Extracorporeal life support (ECLS) systems are life-saving devices used for treating patients with severe cardiopulmonary failure. In this study, we implemented a rat model of ECLS without the administration of inotropes or vasopressors. METHODS: The rats underwent 5 min of untreated asphyxial cardiac arrest and were resuscitated by ECLS for 30 min. The right external jugular vein and right femoral artery were separately cannulated to the ECLS outflow and inflow, respectively. Thereafter, ECLS was terminated, wounds were closed, and mechanical ventilation was provided for another 90 min. Subsequently, blood gas and hemodynamic analyses were performed. The plasma levels of C-reactive protein (CRP), interleukin (IL)-6, IL-10, and tumor necrosis factor-alpha (TNF-α) were measured 120 min after reperfusion. RESULTS: The metabolic rate of lactate in the group of asphyxial cardiac arrest rescued by ECLS was slow; therefore, the pH at 120 min after reperfusion was significantly lower in this group than that in the group of normal rats treated with ECLS. The hemodynamic data showed no between-group differences. The plasma levels of CRP, IL-6, IL-10, and TNF-α increased after ECLS treatment. CONCLUSIONS: We successfully established a rodent ECLS model, which might be a useful approach for studying the pathophysiology induced by ECLS under clinical conditions. ELECTRONIC SUPPLEMENTARY MATERIAL: The online version of this article (doi:10.1186/s12872-017-0558-6) contains supplementary material, which is available to authorized users. BioMed Central 2017-05-15 /pmc/articles/PMC5433070/ /pubmed/28506218 http://dx.doi.org/10.1186/s12872-017-0558-6 Text en © The Author(s). 2017 Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. 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 Article
Chang, Ru-Wen
Luo, Chien-Ming
Yu, Hsi-Yu
Chen, Yih-Sharng
Wang, Chih-Hsien
Investigation of the pathophysiology of cardiopulmonary bypass using rodent extracorporeal life support model
title Investigation of the pathophysiology of cardiopulmonary bypass using rodent extracorporeal life support model
title_full Investigation of the pathophysiology of cardiopulmonary bypass using rodent extracorporeal life support model
title_fullStr Investigation of the pathophysiology of cardiopulmonary bypass using rodent extracorporeal life support model
title_full_unstemmed Investigation of the pathophysiology of cardiopulmonary bypass using rodent extracorporeal life support model
title_short Investigation of the pathophysiology of cardiopulmonary bypass using rodent extracorporeal life support model
title_sort investigation of the pathophysiology of cardiopulmonary bypass using rodent extracorporeal life support model
topic Research Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5433070/
https://www.ncbi.nlm.nih.gov/pubmed/28506218
http://dx.doi.org/10.1186/s12872-017-0558-6
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