Immediate effective allograft function is essential for successful lung transplantation. Yet, despite progress in lung preservation and improvements in surgical techniques and perioperative care, primary graft failure (PGF) continues to be a significant cause of early morbidity and mortality.1– The incidence of PGF has been reported to occur in 13 to 35% of lung transplant recipients.2– The clinical spectrum of early graft dysfunction ranges from mild hypoxemia with associated radiographic infiltrates to full-blown ARDS with hemodynamic instability manifesting within 24 h following the transplant procedure. In addition, histopathologic specimens of lung tissue from patients experiencing severe graft dysfunction reveal nonspecific diffuse alveolar damage. Thus, PGF represents a syndrome consisting of elevated pulmonary vascular resistance, pulmonary edema, and hypoxemia. Although a number of expressions have been used to describe this syndrome, the term primary graft failure has evolved to describe post-transplantation ischemia-reperfusion injury.3 Some of the identified risk factors include prolonged graft ischemia time, increasing donor age, recipient diagnosis of pulmonary hypertension, and use of cardiopulmonary bypass.4–6 However, another group reported no increase in mortality for patients with prolonged graft ischemia time or recipient diagnosis.7 Thus, the unpredictable nature and increased mortality of PGF have created a need to better understand the mechanism of ischemia-reperfusion lung injury.