Pulmonary reperfusion injury is a clinical syndrome with no single and recognized pathophysiologic mechanism. It is a ma-jor cause of morbidity and mortality fol-lowing lung transplantation, cardiogenic shock, or cardiopulmonary bypass. The underlying mechanisms remain uncertain. Lung inflammatory injury induced by li-popolysaccharide, characterized by rapid sequestration of neutrophils in response to inflammatory chemokines and cytokines released in the lungs is an acceptable the-ory. Structural or functional impairment of surfactant has been noted in pulmo-nary reperfusion injury. The pathological changes may include bilateral pulmonary infiltrates, reduced lung compliance and worsening of gas exchange in the imme-diate posttransplant period. Recruitment maneuver and high positive end-expir-atory pressure can relieve postoperative respiratory failure, especially in the pa-tient with reperfusion pulmonary edema after pulmonary thromboendarterectomy. Pharmaceutical agents, including inhaled nitric oxide, soluble complement receptor type 1, prostaglandin E1 and exogenous surfactant, attenuate pulmonary reperfu-sion injury through distinct mechanisms. Extracorporeal membrane oxygenation and Novalung are temporary assistance in bridging to lung transplantation, stabiliza-tion of hemodynamics during transplanta-tion and treatment of severe lung dysfunc-tion and primary graft failure. Modulation of heme oxygenase-1 expression, ischemic conditioning and gene therapy are future directions for pulmonary reperfusion in-jury management.