Postoperative adhesions are a significant source of morbidity, including contributions to pelvic pain, bowel obstruction, and infertility. While the mechanisms of postoperative adhesion development are complex and incompletely understood, hypoxia appears to trigger a cascade of intracellular responses involving hypoxia-inducible factors, lactate, reactive oxygen species, reactive nitrogen species, and insulin-like growth factors that results in manifestation of the adhesion phenotype. Thus, substantial evidence exists to implicate the direct role of cellular metabolism in wound repair and adhesion development.