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Revista brasileira de cirurgia cardiovascular : orgao oficial da Sociedade Brasileira de Cirurgia Cardiovascular

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

يمكن للمستخدمين المسجلين فقط ترجمة المقالات
الدخول التسجيل فى الموقع
يتم حفظ الارتباط في الحافظة
Luiz Dantas de Oliveira Filho
Karen Ruggeri Saad
Paulo Fernandes Saad
Marcia Kiyomi Koike
Sônia Maria da Silva
Edna Frasson de Souza Montero

الكلمات الدالة

نبذة مختصرة

BACKGROUND

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.

CONCLUSIONS

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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