Abstract
To investigate whether N-acetylcysteine, a free radicals scavenger has a protective effect against lung injury as a remote organ after skeletal muscle ischemia-reperfusion. Twenty Wistar male rats were divided randomly into two experimental groups: group ischemia-reperfusion (group I) and group ischemia-reperfusion +N-acetylcysteine (group II). All animals were undergone two hours of ischemia by occlusion femoral artery and 24h of reperfusion. Before clamped the femoral artery, 250 IU heparin was administered via the jugular vein to prevent clotting. Rats that were treated with N-acetylcysteine given IV at a dose of 150 mgkg(-1), immediately before reperfusion. After 24h of reperfusion, animals were euthanized and left lung harvested for histopathological analysis under light microscopy. In the group I, tissues showed histological changes with intra-alveolar edema, intra-alveolar hemorrhage and neutrophilic infiltration. Histopathologically, there was a significant difference (P = 0.005) between two groups. Administration of N-acetylcysteine treatment significantly decreased lung injury induced by skeletal muscle ischemia reperfusion according to histological findings.
Highlights
Many surgical procedures, such as limb revascularization and free-flap reconstruction, involve prolonged ischemia of skeletal muscle
We aimed to examine the protective effect of N-acetylcysteine on lung injury induced by the skeletal muscle ischemia-reperfusion by evaluation of histopathology in rat model
The present study demonstrates that temporary occlusion of the femoral artery of the rats resulted in altered pulmonary endothelial barrier function, with increased protein concentration and neutrophil infiltration
Summary
Many surgical procedures, such as limb revascularization and free-flap reconstruction, involve prolonged ischemia of skeletal muscle. Ischemic damage can lead to severe postoperative complications[1]. There are two components to the reperfusion syndrome, which follows extremity ischemia. The local response follows reperfusion and the systemic response, which results in multiple organ failure and death[2]. Ischemia reperfusion of the lower extremities causes lung injury because of polymorphonuclear sequestration in pulmonary microvasculature, increased endothelial permeability and interstitial edema[3]. Ischemic damage results from a decrease in the blood flow of the organ and reperfusion injury results from the enhanced generation of oxygen radicals[4]
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