Lung donation obtained after carbon monoxide intoxication has been recognized as excellent organs because of less general inflammation and less primary graft dysfunction after procedure. In a murine model of brain dead, carbon monoxide inhalation at a low concentration (50 to 500 parts per million (ppm)) exerts significant cytoprotection in several lung injury models via its vasodilatation, anti-inflammatory, and anti-apoptotic properties (Dong, J Heart Lung transplant, 2010). The carbon monoxide inhalation down-regulates pro-inflammatory cytokines (TNF-alpha, IL-6) along with the increase of anti-inflammatory cytokine (IL-10) in recipient serum. The inhalation significantly decreases cell apoptosis in lung grafts, inhibiting mRNA and protein expression of intercellular adhesion molecule-1 (ICAM-1) and caspase-3 in lung grafts (Zhou, Chin Med J, 2008).