Key result
N-acetylcysteine added to fluid resuscitation cuts cardiac TBARS ~26% and reduces myocardial damage in rats.
Why the study?
Pharmacological therapy is a strategy to prevent complications from ischemia and reperfusion injury after volume replacement in hemorrhagic shock, but the effect of N-acetylcysteine on cardiac injury is unclear.
Does N-acetylcysteine added to fluid resuscitation reduce cardiac injury in a rat hemorrhagic shock model?
RCT
Randomly assigned
Does N-acetylcysteine added to fluid resuscitation reduce cardiac injury in a rat hemorrhagic shock model?
Absolute Event Rate: 0.2% vs 0.27%
p-value: p=0.014
In a rat model of hemorrhagic shock, N-acetylcysteine added to fluid resuscitation attenuated oxidative stress and myocardial damage.
May reduce cardiac oxidative injury in rat hemorrhagic shock; leaves open translation to human resuscitation protocols.
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, 150 mg/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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Filho et al. (2014) conducted an RCT in Hemorrhagic shock. N-acetylcysteine vs. Ringer lactate alone was evaluated on Concentrations of thiobarbituric acid reactive substances (p=0.014). N-acetylcysteine added to fluid resuscitation in a rat hemorrhagic shock model reduced cardiac concentrations of thiobarbituric acid reactive substances (0.20 vs. 0.27, P=0.014) and myocardial damage.
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