Aksu, VolkanYuksel, VolkanChousein, SerchatTastekin, EbruIscan, SahinSagiroglu, GonulCanbaz, Suat2024-06-122024-06-1220151708-53811708-539Xhttps://doi.org/10.1177/1708538114527939https://hdl.handle.net/20.500.14551/21055Purpose We aimed to examine the effects of sildenafil and n-acetylcystein on ischemia/reperfusion injury in femoral artery endothelium and gastrocnemius muscle. Basic methods 32 rats of Sprague-Dawley breed were randomly divided into four groups (n=8). Median laparotomy was performed, then a 120-minute ischemia was created by microvascular clamping of infrarenal aorta, followed by the release of clamping. In sildenafil group, 1mg/kg of sildenafil infusion and in the n-acetylcystein group, 100mg/kg of n-acetylcystein infusion was administered after release of clamps. Blood samples and tissue samples of femoral artery and gastrocnemius muscle were extracted for a histopathological evaluation. Principal findings Serum levels of malondialdehyde in ischemia/reperfusion group (6.160.79) were higher compared to the control group (4.69 +/- 0.33), whereas a significant decrease was detected in sildenafil (5.17 +/- 0.50) and n-acetylcystein (4.96 +/- 0.49) groups. Femoral artery tissue sections of the control group, mean tumor necrosis factor alpha and hypoxy-induced factor-1 alpha immunoreactivity were found to be negative. In the ischemia/reperfusion group, mean tumor necrosis factor immunoreactivity was intense and mean hypoxy-induced factor-1 alpha immunoreactivity was 51-75%. In the ischemia/reperfusion+Sildenafil and ischemia/reperfusion+NAS groups, mean tumor necrosis factor immunoreactivity was slight and mean hypoxy-induced factor-1 alpha immunoreactivity was 26-50%. Conclusions In conclusion, sildenafil and n-acetylcystein may reduce femoral artery endothelium and gastrocnemius muscle injury following lower extremity ischemia/reperfusion.en10.1177/1708538114527939info:eu-repo/semantics/closedAccessFemoral Artery EndotheliumGastrocnemius MuscleIschemiaN-AcetylcysteinReperfusionSildenafilDysfunctionPathophysiologyModelArticle2312130Q4WOS:0003481023000042-s2.0-8492097276224642934Q2