Abstract
To investigate whether N-acetylcysteine has a protective effect against renal injury as a remote organ after skeletal muscle ischemia-reperfusion in rats. Twenty Wistar male rats were divided randomly into two experimental groups: group ischemia-reperfusion (group I) and group ischemia-reperfusion + N-acetylcysteine (group II). After ketamine and xylazine anesthesia, femoral artery was exposed. All animals were undergone 2h of ischemia by occlusion femoral artery and 24h of reperfusion. Rats that were treated with N-acetylcysteine given IV at a dose of 150 mg/kg(-1), immediately before reperfusion. After 24h of reperfusion, the blood samples were collected and submitted for evaluation of plasmatic urea, creatinine values and then rats were euthanized and left kidney harvested for histopathological analysis under light microscopy. The urea (35±7.84 mg.dL(-1)), creatinine (1.46±0.47 mg.dL(-1)) values were significantly lower in group II (P=0.000). Renal histopathologic study in group I showed extensive distal and proximal tubular cells necrosis and sloughing of epithelial cells into the tubular lumen, cast formation in tubule and glomerul, glomerul fibrosis and hemorrhage. Histopathologically, there was a significant difference (p=0.037) between two groups. The N-acetylcysteine was able to decrease renal injury induced by skeletal muscle ischemia reperfusion in rats.
Highlights
Ischemic and reperfusion injury of the extremities may result in a systemic, severe and complex metabolic syndrome, manifested by acute renal failure, myoglobinuria, metabolic acidosis, hypercalemia and free radicals release[1]
We aimed to examine the protective effect of N-acetylcysteine on kidney as a remote organ damage after the skeletal muscle ischemia-reperfusion by assessing histopathological and functional analysis in rat model
Restoring blood flow to the extremities exposed to ischemia can cause the reperfusion injury by leading to formation of oxygen-derived free radicals that lead to more muscle necrosis than that caused by the ischemia itself[16,17]
Summary
Ischemic and reperfusion injury of the extremities may result in a systemic, severe and complex metabolic syndrome, manifested by acute renal failure, myoglobinuria, metabolic acidosis, hypercalemia and free radicals release[1]. The pathogenesis of acute renal failure following rhabdomyolysis has been attributed to several mechanisms: 1) Myoglobin nephrotoxicity impair renal function, mainly when dehydratation, acidemia, or both coxists; 2) Primary reduction of glomerular filtration rate due to cortical and glomerular hemodynamic changes due to hypotension after restoration of the blood flow to the extremity; 3) Myoglobin cast producing tubular obstruction and tubular acute necrosis; 4) Release of oxygenderived free radicals mediating back leakage of filtrate through damaged tubular renal epithelium, with loss of renal excretory function[1] Multiple pharmacological agents such as iloprost, vitamin C, pentoxifylline and L-alanyl-glutamin are proposed to be useful against renal injury as a remote organ after hindlimb ischemia-reperfusion[2,3,4]. Recent clinical trials suggest that N-acetylcysteine may be effective in preventing contrast nephropathy[10,11,12]
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