Abstract
To evaluate the effect of N-acetylcysteine, as a renoprotective agent, when administered early after anesthesia induction, against ischemia/reperfusion injury in rats anesthetized with isoflurane. Eighteen male Wistar rats weighing > 300 g were anesthetized with isoflurane. The internal jugular vein and the left carotid artery were dissected and cannulated. The animals were randomly divided into GAcetyl, receiving intravenous N-acetylcysteine, 300 mg/kg, and GIsot, isotonic saline. After 30 minutes, right nephrectomy was performed and the left renal artery was clamped during 45 minutes. The animals were sacrificed after 48 hours and blood samples were taken after anesthetic induction and upon sacrificing of the animals to evaluate blood creatinine. The kidneys were sent for histological analysis. The variation in serum creatinine was 2.33 mg/dL ± 2.21 in GAcetyl and 4.38 mg/dL ± 2.13 in GIsot (p=0.074). Two animals presented intense tubular necrosis in GAcetyl, compared to 5 in GIsot. Only GAcetyl presented animals free of tubular necrosis (two) and tubular degeneration (one). After renal ischemia/reperfusion, the rats which were given N-acetylcysteine presented less variation in serum creatinine and milder kidney injuries than the control group.
Highlights
Acute renal failure (ARF) has high incidence in intensive care units, representing an isolated prognostic factor in patients with multiple organ and system disorder[1].Reactive oxygen species are normally produced during cell metabolism
The aim of this study was to evaluate the effect of N-acetylcysteine as a renoprotective agent, when administered early after induction, against ischemia/reperfusion injury in rats anesthetized with isoflurane
For the kidneys that suffered ischemia, tubular necrosis was not observed in two GAcetyl kidneys but it was observed in grade II in GAcetyl (4 kidneys) and GIsot (3 kidneys) and grade III in GAcetyl (2 kidneys) and GIsot (5 kidneys) (p = 0.18)
Summary
Reactive oxygen species are normally produced during cell metabolism. Free radicals may affect cell vitality by several mechanisms, interfering in the cell growth and proliferation, regeneration and tissue repair, inflammatory response and immune process. Nitric oxide and the peroxynitrite radical present the capacity to induce oxidation damage[2]. Kidneys are responsible for 10% of the body oxygen consumption. They are physiological sources of free radicals, especially stemming from the tubular metabolism[3]. This production increases during the tissue insult process and may contribute towards the installation and progression of the kidney injury[4]
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