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Journal of Surgical Research 2016-Jun

N-acetylcysteine reduces the renal oxidative stress and apoptosis induced by hemorrhagic shock.

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Miriam Aparecida Moreira
Maria Claudia Irigoyen
Karen Ruggeri Saad
Paulo Fernandes Saad
Marcia Kiyomi Koike
Edna Frasson de Souza Montero
José Luiz Martins

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Renal ischemia/reperfusion injury induced by hemorrhagic shock (HS) and subsequent fluid resuscitation is a common cause of acute renal failure. The objective of this study was to evaluate the effect of combining N-acetylcysteine (NAC) with fluid resuscitation on renal injury in rats that underwent HS.

Two groups of male Wistar rats were induced to controlled HS at 35 mm Hg mean arterial pressure for 60 min. After this period, the HS and fluid resuscitation (HS/R) group was resuscitated with lactate containing 50% of the blood that was withdrawn. The HS/R + NAC group was resuscitated with Ringer's lactate combined with 150 mg/kg of NAC and blood. The sham group animals were catheterized but were not subjected to shock. All animals were kept under anesthesia and euthanized after 120 min of fluid resuscitation or observation.

Animals treated with NAC presented attenuation of histologic lesions, reduced oxidative stress, and apoptosis markers when compared with animals from the HS/R group. The serum creatinine was similar in all the groups.

NAC is a promising drug for combining with fluid resuscitation to attenuate the kidney injury associated with HS.

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