論文

国際誌
2010年6月

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

The Annals of thoracic surgery
  • Tomokazu Kakishita
  • Takahiro Oto
  • Shiro Hori
  • Kentaroh Miyoshi
  • Shinji Otani
  • Sumiharu Yamamoto
  • Naohisa Waki
  • Osamu Yoshida
  • Mikio Okazaki
  • Masaomi Yamane
  • Shinichi Toyooka
  • Yoshifumi Sano
  • Shinichiro Miyoshi
  • 全て表示

89
6
開始ページ
1773
終了ページ
9
記述言語
英語
掲載種別
研究論文(学術雑誌)
DOI
10.1016/j.athoracsur.2010.02.077

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-alpha and interleukin 8 levels were elevated in the perfusate 2 hours after perfusion. Although tumor necrosis factor-alpha 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-alpha 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.

リンク情報
DOI
https://doi.org/10.1016/j.athoracsur.2010.02.077
PubMed
https://www.ncbi.nlm.nih.gov/pubmed/20494026
ID情報
  • DOI : 10.1016/j.athoracsur.2010.02.077
  • PubMed ID : 20494026

エクスポート
BibTeX RIS