Abdominal ischemia-reperfusion (I/R) is known to cause both structural and functional damage to sciatic nerve which is related to the oxidative stress. We investigated the protective effects of mitochondria-targeted antioxidant (2-(2,2,6,6-tetramethylpiperidin-1-oxyl-4-ylamino)-2-oxoethyl) triphenylphosphonium chloride (MitoTEMPO) on ischemia-reperfusion-induced nerve damage by using the conduction velocity distribution (CVD) calculations from in vitro compound nerve action potential (CNAP) recordings from rat sciatic nerve. Adult male Wistar albino rats were divided into three groups. The IR and IR + MT groups had aortic cross-clamping for 1 h followed by 2 h reperfusion, while SHAM group had the same procedure without cross-clamping. IR + MT group received 0.7 mg/kg/day MitoTEMPO injection for 28 days before I/R, while other groups received vehicle alone. Ischemia-reperfusion resulted in a significant decrease (p < .05) in maximum depolarizations (mV), areas (mV.ms), and maximum and minimum upstroke velocities (mV/ms) of CNAPs, while injection of MitoTEMPO showed a complete protective effect on these impairments. The histograms for CVD showed that I/R blocked the contribution of fast-conducting fibers (> 60 m/s). MitoTEMPO prevented that blockage and caused a shift in the CVD. Functional nerve damage caused by I/R can be prevented by MitoTEMPO, which can enter mitochondria, the main source of reactive oxygen species (ROS).