Chronic ischemic wounds presenting at wound clinics are heterogeneous with respect to etiology, age of the wound and other factors complicating wound healing. In addition, there are ethical challenges associated with collecting repeated biopsies from a patient to develop an understanding of the temporal dynamics of the mechanisms underlying chronic wounds. The need for a pre-clinical model of ischemic wound is therefore compelling. The porcine model is widely accepted as an excellent pre-clinical model for human wounds. A full-thickness bipedicle flap approach was adopted to cause skin ischemia. Closure of excisional wounds placed on ischemic tissue was severely impaired resulting in chronic wounds. Histologically, ischemic wounds suffered from impaired re-epithelialization, delayed macrophage recruitment and poorer endothelial cell abundance and organization. Compared to the pair-matched non-ischemic wound, unique aspects of the ischemic wound biology were examined on days 3, 7, 14 and 28 by systematic screening of the wound tissue transcriptome using high-density porcine GeneChips^TM. Ischemia markedly potentiated the expression of arginase-1, a cytosolic enzyme that metabolizes the precursor of nitric oxide L-arginine. Ischemia also induced the SOD2 in the wound tissue perhaps as survival response of the challenged tissue. Human chronic wounds also demonstrated elevated expression of SOD2 and arginase-1. This study provides a thorough database which may serve as a valuable reference tool to develop novel hypotheses aiming to elucidate the biology of ischemic chronic wounds in a pre-clinical setting.