T he most significant factor limiting lung transplan- tation is the availability of suitable donors. Cur- rently, fewer than half of the patients listed for lung transplantation will have a suitable donor available. 1 Most potentially available lung donors are brain-dead patients, 2 although the recent use of donors that are not brain dead, or donors after cardiac death (DCD), 3 has provided a new source of potential organs suitable for transplantation. In 2007, the Organ Procurement and Transplanta- tion Network reported 22 048 solid organs transplanted from 8091 deceased donors. 1 From those donors, only 1465 lung transplants (18%) were performed. The fac- tors precluding the use of lungs for transplantation are many. Deceased donors are exposed to many inflam- matory events associated with brain death, including possible aspiration of gastric contents, blood, or upper airway secretions, the effects of endotracheal intuba- tion and exposure to mechanical ventilation, and the likelihood of ventilator-associated infection, as well as the possibility of neurogenic pulmonary edema. 2 In addition, brain death induces disruption in homeostatic regulation with secondary disturbances in endocrine function and inflammatory reactions, hypothermia, and coagulopathy. 4 Complex mechanisms may be involved in deteri- oration of gas exchange in brain-dead donors. Neuro- genic pulmonary edema is common in brain-dead organ donors. Rogers et al 5 reported that patients who died of head injury consistently had higher lung weights on autopsy and concluded that every patient with a head injury has some degree of neurogenic pulmonary edema. In a sheep model of increased intracranial pres- sure, Peterson et al 6 demonstrated a modest increase in Effects of administration of intravenous naloxone on gas exchange in brain-dead lung donors Objective—To observe the effect of naloxone on the lung function of potential lung transplant donors with neurogenic pulmonary edema. Design and Interventions—Donors aged 16 to 55 years without any factors to contraindicate lung donation (pneumonia, pulmonary contusion, etc) were included. Ventilator settings were standardized to a tidal volume of 10 to 12 mL/kg, an FIO 2 of 0.40, and a respiratory rate that kept PCO 2 between 35 and 45 mm Hg. Chest physiotherapy, nebulizer treatments, and frequent suctioning were undertaken. Baseline arterial blood gas analysis and an oxygen challenge were performed. The patients were then given 8 to 10 mg of naloxone. Oxygen challenges and arterial blood gas analyses were repeated every 4 to 6 hours. The data were analyzed by using a paired t test, and each patient served as his or her own control. Setting—These interventions were performed on the 19 LifeQuest donors who met the set criteria from July 2002 to July 2004. Results—The PaO 2 on the oxygen challenge immediately after administration of naloxone increased from 329 (SD 177) to 363 (SD 191) mm Hg, although the increase from baseline was not significant. The PaO 2 from the second oxygen challenge (median time, 7 hours after administration of naloxone) increased to 413 (SD 177) mm Hg (P < .01). (Progress in Transplantation. 2009;19:267-271) Christina Eagan, RN, BSN, CPTC, Cesar A. Keller, MD, Maher A. Baz, MD, Michael Thibault, RN, BSN, CPTC LifeQuest Organ Recovery Services, Gainesville, Florida (CE, MT), Mayo Clinic, Jacksonville, Florida (CAK), University of Florida College of Medicine, Gainesville, Florida (MAB) Corresponding author: Christina Eagan, RN, BSN, CPTC, Advanced Practice Coordinator, LifeQuest Organ Recovery Services, 720 SW 2nd Ave, Suite 570, Gainesville, FL 32601 (e-mail: eaganc@lifequest.ufl.edu) To purchase electronic or print reprints, contact: The InnoVision Group 101 Columbia, Aliso Viejo, CA 92656 Phone (800) 809-2273 (ext 532) or (949) 448-7370 (ext 532) Fax (949) 362-2049 E-mail reprints@aacn.org 267 Progress in Transplantation, Vol 19, No. 3, September 2009