The use of non-heart-beating donor (NHBD) lungs may help to overcome the shortage of lung grafts in clinical
lung transplantation, but warm ischaemia and ischaemia/
reperfusion injury (I/R injury) resulting in
primary graft dysfunction represent a considerable threat. Thus, better strategies for optimized preservation of lung grafts are urgently needed.
Surfactant dysfunction has been shown to contribute to I/R injury, and
surfactant replacement
therapy is effective in enhancing lung function and structural integrity in related rat models. In the present study we hypothesize that
surfactant replacement
therapy reduces oedema formation in a pig model of NHBD
lung transplantation. Oedema formation was quantified with (SF) and without (non-SF)
surfactant replacement
therapy in interstitial and alveolar compartments by means of design-based stereology in NHBD lungs 7 h after
cardiac arrest, reperfusion and
transplantation. A
sham-operated group served as control. In both NHBD groups, nearly all animals died within the first hours after
transplantation due to right
heart failure. Both SF and non-SF developed an interstitial oedema of similar degree, as shown by an increase in septal wall volume and arithmetic mean thickness as well as an increase in the volume of peribron-chovascular connective tissue. Regarding intra-alveolar oedema, no statistically significant difference could be found between SF and non-SF. In conclusion,
surfactant replacement
therapy cannot prevent poor outcome after prolonged warm ischaemia of 7 h in this model. While the beneficial effects of
surfactant replacement
therapy have been observed in several experimental and clinical studies related to heart-beating donor lungs and cold ischaemia, it is unlikely that
surfactant replacement
therapy will overcome the shortage of organs in the context of prolonged warm ischaemia, for example, 7 h. Moreover, our data demonstrate that right heart function and dysfunctions of the pulmonary vascular bed are limiting factors that need to be addressed in NHBD.