Ischemia-reperfusion injury induces endothelial dysfunction related to oxidative stress and a lack of nitric oxide bioavailability. The non-invasive forearm ischemia-reperfusion model is commonly used to evaluate interventions to attenuate decrements in brachial artery endothelial function. To date, no study has evaluated the impact of an ischemia-reperfusion injury on the mechanics of the brachial artery, which should also be altered by this injury. 10 healthy participants (6 male, 4 female) underwent ischemia-reperfusion injury (IRI) on 2 separate visits to the laboratory. The first visit provided control measurements, in the absence of supplements. One hour prior to the second visit, participants took 1200mg Ibuprofen (cyclooxygenase inhibitor). IRI was induced by a 20 minute upper-arm supra-systolic occlusion. Measures of brachial artery stiffness were made immediately before, and then 15, 30 and 45 minutes post-IRI. Brachial artery stiffness was determined by non-invasive ultrasound assessment of arterial diameter using echo tracking software at 2MHz (Hitachi Aloka Alpha 6). Arterial perfusion pressures were measured by applanation tonometry on the contralateral radial artery. Immediately prior to each measure the tonometer was calibrated to contralateral brachial artery pressures using an oscillometric sphygmomanometer. Values are mean ± SD. Significance was assessed at 95% confidence levels using two-way repeated-measures ANOVA (SPSS v19). Results show that IRI did not significantly change arterial compliance (Control Pre: 0.06±0.02; Post 15: 0.08±0.02; Post 30: 0.08±0.03; Post 45: 0.07±0.03; and Ibuprofen Pre: 0.07±0.03; Post 15: 0.07±0.03; Post 30: 0.07±0.03; Post 45: 0.07±0.03 mm2/kPa) from baseline over time or between conditions (p=0.55, p=0.65, respectively). Similarly, IRI and Ibuprofen intake had no significant effect on change in arterial diameter (p=0.93 and p=0.43, respectively) and pulse pressure (p=0.39 and p=0.97, respectively). These data demonstrate neither detrimental effect of IRI, nor palliative effect of Ibuprofen before or after IRI, at the brachial artery. It seems that reduced nitric oxide bioavailability as a result of IRI and prostaglandin inhibition by Ibuprofen have no effect on the mechanical properties of a muscular peripheral artery such as the brachial artery in apparently healthy individuals.