Oxidative stress, a major contributor to brain damage in ischemic stroke, is involved in alterations of cerebrovascular properties after an episode of ischemia/reperfusion. (Jiménez-Altayó F et al., 2009). Uric acid (UA) is an endogenous antioxidant that protects the rat brain in a model of thromboembolic (Romanos E et al., 2007) and transient focal (Yu et al., 1998) ischemic injury. Nevertheless, little is known about the mechanisms whereby UA exerts its beneficial effects. We hypothesized that UA could influence the changes on vessel properties due to ischemia/reperfusion. Male Sprague-Dawley rats (270-320g) were subjected to right middle cerebral artery (MCA) intraluminal occlusion (90 min) followed by 24 h reperfusion. Sham-operated animals underwent the same surgical procedure but the MCA was occluded for less than 1 min. Rats were anaesthetized with isoflurane (3-2.5 %) in a mixture of O2 and N2O (30:70) and divided into 4 groups: sham-operated vehicle (n=7), ischemic vehicle (IV, n=18), sham-operated UA (n=4) and ischemic UA (IUA, n=9). UA (16 mg/kg in 3 ml Locke’s buffer, i.v.) or vehicle (3 ml Locke’s buffer, i.v.) was infused during 20 min at 30 min reperfusion. Mean arterial pressure, rectal temperature and cortical cerebral blood flow was permanently monitored. Afterwards (24 h), rats were killed under isoflurane (4%) and the ipsilateral MCA was removed and set up in a pressure myograph under physiological conditions. Values are means ± S.E.M., compared by two-way ANOVA or Student’s t-Test. Mean arterial blood pressure (IV: 94.7±1.6 mmHg, n=18; IUA: 91.3±1.0 mmHg, n=9) and rectal temperature (IV: 37.3±0.119 °C, n=18; IUA: 37.0±0.197 °C, n=9) was similar in all groups. UA reduced infarct volume (IV: 129.6±23.5 mm3, n=18; IUA: 48.9±16.6 mm3, n=9, p<0.01), neurological score (IV: 3.4±0.4, n=18; IUA: 2.0±0.3, n=9, p<0.05) and brain oedema (IV: 7.7±1.1, n=16; IUA: 2.9±1.4, n=7, p<0.05). Ischemia/reperfusion increased MCA wall thickness (p<0.01), cross-sectional area (p<0.05) and wall/lumen ratio (p<0.05) while decreased wall stress (p<0.05) and stiffness (β value SV: 7.8±0.1, n=5; β value IV: 6.8±0.2, n=17, p<0.001). UA prevented all MCA changes induced by ischemia/reperfusion. These results show that a single dose of UA administered early after the onset of reperfusion prevents MCA structural and mechanical alterations induced by ischemia/reperfusion. We suggest that UA might exert beneficial actions on ischemic damage through prevention of cerebrovascular remodelling. These results reinforce the involvement of the vascular response in brain damage.