Effect of N-acetylcysteine in hearts of rats submitted to controlled
hemorrhagic shock |
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Authors: | Luiz Dantas de Oliveira Filho Karen Ruggeri Saad Paulo Fernandes Saad Marcia Kiyomi Koike S?nia Maria da Silva Edna Frasson de Souza Montero |
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Institution: | 1. Universidade Federal de São Paulo (UNIFESP), São Paulo, SP, Brazil.;2. Universidade Federal do Vale do São Francisco (UNIVASF), Petrolina, PE, Brazil.;3. Faculdade de Medicina da Universidade de São Paulo (FMUSP), São Paulo, SP, Brazil. |
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Abstract: | IntroductionPharmacological 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.ObjectiveThe 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.MethodsMice 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.ResultsCardiac 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.ConclusionThe 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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Keywords: | Shock Hemorrhagic Heart Acetylcysteine Oxidative Stress Inflammation |
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