Lung transplantation is now considered part of the routine management of end-stage pulmonary diseases. Early approaches for improving the short-and long-term outcomes were in the area of technical aspects of the operation and of immunosuppression. However, since these initial improvements, there have been no significant changes in regard to early postoperative mortality or long-term survival.(1) In particular, the development of PGF remains a difficult problem in the early postoperative period and still occurs in 15% to 20% of transplants.(1,2) It is a significant cause of early postoperative mortality as well as a major contributor to the development of late complications. The clinical scenario of PGF is characterized by the rapid onset of severe hypoxemia, pulmonary edema, and decreased lung compliance, often followed by multisystem organ failure. This may occur within hours to days of the transplantation and may occur in one or both transplanted lungs. PGF is associated with a high mortality rate. Among survivors, it results in lengthy hospitalization and prolonged recovery among survivors. In fact, PGF is a major reason for the perioperative mortality rate of 15%, which has remained unchanged despite advances in other areas of lung transplantation.(1,2) There is no clear pathogenesis for PGF; it appears unrelated to age, underlying pulmonary disease, preoperative pulmonary artery pressures, type of transplant, allograft ischemic times, use of cardiopulmonary bypass, or use of PGE(1) infusion.(2) It mimics the clinical course of adult respiratory distress syndrome, and the mechanism of injury may be very similar. In an effort to minimize the development of PGF, attention needs to be focused on lung preservation to reduce the impact of explantation, ischemia, and reperfusion on the transplanted lung. In addition, improved preservation techniques would extend permissible ischemic times, make more distant procurement of donor lungs possible, and allow HLA cross-matching.