Suppression of inflammatory cytokines during ex vivo lung perfusion with an adsorbent membrane

T Kakishita, T Oto, S Hori, K Miyoshi, S Otani… - The Annals of thoracic …, 2010 - Elsevier
T Kakishita, T Oto, S Hori, K Miyoshi, S Otani, S Yamamoto, N Waki, O Yoshida, M Okazaki
The Annals of thoracic surgery, 2010Elsevier
BACKGROUND: Lung grafts can be perfused ex vivo for 2 hours without edema formation;
however, prolonged ex vivo lung perfusion (EVLP) eventually induces lung injury. This study
evaluated the change in proinflammatory cytokines of the perfusate during EVLP and
investigated the effect of cytokine removal using an adsorbent membrane. METHODS:
Porcine heart-lung blocks were harvested after electrically induced cardiac arrest and
underwent 12-hour EVLP with an adsorbent membrane (membrane group: n= 5) and …
BACKGROUND
Lung grafts can be perfused ex vivo for 2 hours without edema formation; however, prolonged ex vivo lung perfusion (EVLP) eventually induces lung injury. This study evaluated the change in proinflammatory cytokines of the perfusate during EVLP and investigated the effect of cytokine removal using an adsorbent membrane.
METHODS
Porcine heart-lung blocks were harvested after electrically induced cardiac arrest and underwent 12-hour EVLP with an adsorbent membrane (membrane group: n = 5) and without an adsorbent membrane (control group: n = 6).
RESULTS
In the control group, both tumor necrosis factor-α and interleukin 8 levels were elevated in the perfusate 2 hours after perfusion. Although tumor necrosis factor-α and interleukin 8 levels were significantly lower in the membrane group than in the control group during the EVLP period, there was no significant difference in oxygenation, pulmonary vascular resistance, edema formation, or myeloperoxidase activity between the two groups.
CONCLUSIONS
Tumor necrosis factor-α and interleukin 8 levels of the perfusate were elevated during EVLP. Although adverse effects of these inflammatory cytokines were anticipated, removal of inflammatory cytokines by the adsorbent membrane did not improve lung function during prolonged EVLP. Factors other than the cytokines may play a major role in causing lung injury during EVLP. Further research is needed to investigate the real mechanism of lung graft injury during prolonged EVLP and to establish longer EVLP duration for graft treatment. This strategy could contribute to the salvage of potentially damaged lungs, especially from cardiac death donors, and to expansion of the donor pool.
Elsevier