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Effect of N-acetylcysteine in hearts of rats submitted to controlled hemorrhagic shock

INTRODUCTION: Pharmacological therapy is a strategy for the prevention of complications associated with ischemia and reperfusion injury that occurs after volume replacement in the treatment of hemorrhagic shock. OBJECTIVE: The aim of this study was to evaluate the effect of N-acetylcysteine associat...

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Autores principales: de Oliveira Filho, Luiz Dantas, Saad, Karen Ruggeri, Saad, Paulo Fernandes, Koike, Marcia Kiyomi, da Silva, Sônia Maria, Montero, Edna Frasson de Souza
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Sociedade Brasileira de Cirurgia Cardiovascular 2015
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4462962/
https://www.ncbi.nlm.nih.gov/pubmed/26107448
http://dx.doi.org/10.5935/1678-9741.20140097
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author de Oliveira Filho, Luiz Dantas
Saad, Karen Ruggeri
Saad, Paulo Fernandes
Koike, Marcia Kiyomi
da Silva, Sônia Maria
Montero, Edna Frasson de Souza
author_facet de Oliveira Filho, Luiz Dantas
Saad, Karen Ruggeri
Saad, Paulo Fernandes
Koike, Marcia Kiyomi
da Silva, Sônia Maria
Montero, Edna Frasson de Souza
author_sort de Oliveira Filho, Luiz Dantas
collection PubMed
description INTRODUCTION: Pharmacological therapy is a strategy for the prevention of complications associated with ischemia and reperfusion injury that occurs after volume replacement in the treatment of hemorrhagic shock. OBJECTIVE: The aim of this study was to evaluate the effect of N-acetylcysteine associated with fluid resuscitation in cardiac injury in a rat hemorrhagic shock model. METHODS: Mice Wister male rats were randomly and subjected to controlled hemorrhagic shock for 60 min. and then, subjected to resuscitation with Ringer lactate. In a group of six animals, 150mg/kg of N-acetylcysteine were added to fluid volume replacement. The animals were observed for 120 min and after this period, were euthanized and cardiac tissue was collected for histopathological analysis and measurement of thiobarbituric acid reactive substances and pro-and anti-inflammatory interleukin. RESULTS: Cardiac tissue of the group treated with N-acetylcysteine showed lower concentrations of thiobarbituric acid reactive substances (0.20±0.05 vs. 0.27±0.05, P=0.014) and reduced histopathological damage and edema when compared to the group whose volume replacement occurred only with Ringer lactate. There was no difference in the expression of cytokines interleukin 6 (2,138.29±316.89 vs. 1,870.16±303.68, P=0.091) and interleukin 10 (1.019,83±262,50 vs. 848.60±106.5, P=0.169) between the treated groups. CONCLUSION: The association of N-acetylcysteine on volume replacement attenuates oxidative stress in the heart, as well myocardial damage and edema, but does not modify the expression of inflammatory cytokines.
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spelling pubmed-44629622015-06-15 Effect of N-acetylcysteine in hearts of rats submitted to controlled hemorrhagic shock de Oliveira Filho, Luiz Dantas Saad, Karen Ruggeri Saad, Paulo Fernandes Koike, Marcia Kiyomi da Silva, Sônia Maria Montero, Edna Frasson de Souza Rev Bras Cir Cardiovasc Original Articles INTRODUCTION: Pharmacological therapy is a strategy for the prevention of complications associated with ischemia and reperfusion injury that occurs after volume replacement in the treatment of hemorrhagic shock. OBJECTIVE: The aim of this study was to evaluate the effect of N-acetylcysteine associated with fluid resuscitation in cardiac injury in a rat hemorrhagic shock model. METHODS: Mice Wister male rats were randomly and subjected to controlled hemorrhagic shock for 60 min. and then, subjected to resuscitation with Ringer lactate. In a group of six animals, 150mg/kg of N-acetylcysteine were added to fluid volume replacement. The animals were observed for 120 min and after this period, were euthanized and cardiac tissue was collected for histopathological analysis and measurement of thiobarbituric acid reactive substances and pro-and anti-inflammatory interleukin. RESULTS: Cardiac tissue of the group treated with N-acetylcysteine showed lower concentrations of thiobarbituric acid reactive substances (0.20±0.05 vs. 0.27±0.05, P=0.014) and reduced histopathological damage and edema when compared to the group whose volume replacement occurred only with Ringer lactate. There was no difference in the expression of cytokines interleukin 6 (2,138.29±316.89 vs. 1,870.16±303.68, P=0.091) and interleukin 10 (1.019,83±262,50 vs. 848.60±106.5, P=0.169) between the treated groups. CONCLUSION: The association of N-acetylcysteine on volume replacement attenuates oxidative stress in the heart, as well myocardial damage and edema, but does not modify the expression of inflammatory cytokines. Sociedade Brasileira de Cirurgia Cardiovascular 2015 /pmc/articles/PMC4462962/ /pubmed/26107448 http://dx.doi.org/10.5935/1678-9741.20140097 Text en http://creativecommons.org/licenses/by-nc/3.0/ This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.
spellingShingle Original Articles
de Oliveira Filho, Luiz Dantas
Saad, Karen Ruggeri
Saad, Paulo Fernandes
Koike, Marcia Kiyomi
da Silva, Sônia Maria
Montero, Edna Frasson de Souza
Effect of N-acetylcysteine in hearts of rats submitted to controlled hemorrhagic shock
title Effect of N-acetylcysteine in hearts of rats submitted to controlled hemorrhagic shock
title_full Effect of N-acetylcysteine in hearts of rats submitted to controlled hemorrhagic shock
title_fullStr Effect of N-acetylcysteine in hearts of rats submitted to controlled hemorrhagic shock
title_full_unstemmed Effect of N-acetylcysteine in hearts of rats submitted to controlled hemorrhagic shock
title_short Effect of N-acetylcysteine in hearts of rats submitted to controlled hemorrhagic shock
title_sort effect of n-acetylcysteine in hearts of rats submitted to controlled hemorrhagic shock
topic Original Articles
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4462962/
https://www.ncbi.nlm.nih.gov/pubmed/26107448
http://dx.doi.org/10.5935/1678-9741.20140097
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