Donor lung ventilation and inflation during the
warm ischemia could attenuate
ischemia-reperfusion injury (IRI) after
lung transplantation.
Hydrogen sulfide (H2S), as a kind of protective gas, has demonstrated the antilung IRI effect. This study is aimed at observing the different methods of administering H2S in the setting of
warm ischemia, ventilation, and inflation on the lung graft from a rat non-heart-beating donor. After 1 h of
cardiac arrest, donor lungs in situ were inflated with 80 ppm H2S (FS group), ventilated with 80 ppm H2S (VS group), or deflated (control group) for 2 h. Then, the
lung transplantation was performed after 3 h cold ischemia. The rats without
ischemia and reperfusion were in the
sham group.
Pulmonary surfactant in the bronchoalveolar lavage fluid was measured in donor lung. The inflammatory response, cell apoptosis, and lung graft function were assessed at 3 h after reperfusion. The
lung injury was exacerbated in the control group, which was attenuated significantly after the H2S treatment. Compared with the FS group, the
pulmonary surfactant in the donor was deteriorated, the lung oxygenation function was decreased, and the inflammatory response and cell apoptosis were increased in the graft in the VS group (P < 0.05). In conclusion, H2S inflation during the
warm ischemia phase improved the function of lung graft via regulating
pulmonary surfactant stability and decreased the lung graft IRI via decreasing the inflammatory response and cell apoptosis.