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

Revista Brasileira de Cirurgia Cardiovascular

Luiz Dantas De Oliveira Filho¹  Karen Ruggeri Saad¹  Paulo Fernandes Saad¹  Marcia Kiyomi Koike¹  Sônia Maria Da Silva¹  Edna Frasson De Souza Montero¹ 

关键词: Shock;    Hemorrhagic;    Heart;    Acetylcysteine;    Oxidative Stress;    Inflammation;    Choque Hemorrágico;    Coração;    Acetilcisteína;    Estresse Oxidativo;    Inflamação;   

DOI  :  10.5935/1678-9741.20140097

来源: SciELO

【 摘 要 】

AbstractIntroduction: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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