The pain mechanism in ischemic conditions like intermittent claudication is poorly understood, partly due to the lack of suitable chronic pre-clinical models. In the present study we modified an existing model of ischemia (Orito et al., 2004) in an effort to develop a better characterized chronic ischemic pain model. Since ischemia reduces pH in the affected tissues and TRPV1 channels transduce pH changes, we also studied the role of TRPV1 in this model. Baseline heat (Hargreave's) and mechanical (von Frey) thresholds were measured in the hindpaws of male Sprague-Dawley rats, and they were trained to run on a treadmill with an electric shock-grid. Left iliac artery of the rats was then surgically occluded and animals were allowed to recover for 48h. At 48h, 72h, and weekly from 1wk through 8wk, heat and mechanical thresholds were measured again. Animals were then placed on the treadmill and forced to run for 5 min using mild electric shock motivation. Pain behavior was measured as i) onset time for lifting, shaking or dragging the hind limb; ii) incapacity of the animal to run on the treadmill, indicated by the number of hits on the shock-grid; iii) reduction in heat and/or mechanical threshold after treadmill test. Our results show that the onset time for exercise-induced pain was shorter, number of hits on shock-grid was higher, and the mechanical threshold was reduced (mechanical allodynia) in ligated animals compared to sham. The pain behavior was present for 3-6 weeks with peak at 48-72h. Preliminary results show that at 72h time-point, TRPV1 antagonist capsazepine (25 mg/kg.,i.p.) increased the capacity of the ligated animals to run, but did not affect the onset of pain or allodynia, indicating a role for TRPV1 receptors in this model. Studies are underway to further characterize the model and to confirm the preliminary findings.