Suppression of Inflammatory Cytokines During Ex Vivo Lung Perfusion With an Adsorbent Membrane
Suppression of Inflammatory Cytokines During Ex Vivo Lung Perfusion With an Adsorbent Membrane
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DOI：
10.1016/j.athoracsur.2010.02.077
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发表时间：
2010-06-01
影响因子：
4.6
通讯作者：
Miyoshi, Shinichiro
中科院分区：
文献类型：
--
作者：
Kakishita, Tomokazu;Oto, Takahiro;Miyoshi, Shinichiro
背景肺移植物可以离体灌注2小时而不形成水肿;然而，延长的离体肺灌注（EVLP）最终诱导肺损伤。本研究评价了EVLP期间灌流液中促炎细胞因子的变化，并研究了使用吸附膜去除细胞因子的效果。电诱导心脏停搏后，收集猪心肺组织块，进行12 h EVLP，膜组（n = 5）和对照组（n = 6）分别采用吸附膜和非吸附膜进行EVLP。在对照组中，灌注后2小时，灌注液中的肿瘤坏死因子-α和白细胞介素8水平均升高。尽管EVLP期间膜组的肿瘤坏死因子-α和白细胞介素8水平显著低于对照组，但两组之间的氧合、肺血管阻力、水肿形成或髓过氧化物酶活性无显著差异。在EVLP过程中，灌注液的肿瘤坏死因子-α和白细胞介素8水平升高。虽然预期这些炎性细胞因子的不良反应，但通过吸附膜去除炎性细胞因子并不能改善延长EVLP期间的肺功能。细胞因子以外的因素可能在EVLP期间引起肺损伤中起主要作用。需要进一步研究延长EVLP期间肺移植物损伤的真实的机制，并建立更长的EVLP治疗时间。这种策略可能有助于挽救潜在受损的肺，特别是来自心脏死亡供体的肺，并扩大供体库。(Ann Thorac Surg 2010; 89：1773-81）（C）2010年，胸外科医师协会
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. (Ann Thorac Surg 2010; 89: 1773-81) (C) 2010 by The Society of Thoracic Surgeons