The maximum dimension of the consolidation was an independent unfavourable prognostic factor, regardless of the maximum tumour dimension. This could lead to the more accurate prediction of pathological lymph node metastasis with both GGO and consolidation.
Objective: Improvement in ex vivo lung perfusion (EVLP) protocols could increase the number of donors available for transplantation and protect the lungs from primary graft dysfunction. We hypothesize that perfusate adsorption during EVLP reconditions the allograft to ischemia-reperfusion injury after lung transplantation. Methods: Donor pig lungs were preserved for 24h at 4°C, followed by 6h of EVLP according to the Toronto protocol. The perfusate was additionally adsorbed through a CytoSorb adsorber in the treatment group, whereas control lungs were perfused according to the standard protocol (n = 5, each). EVLP physiology and biochemistry were monitored. Upon completion of EVLP, a left single lung transplantation was performed. Oxygenation function and lung mechanics were assessed during a 4-hour reperfusion period. The inflammatory response was determined during EVLP and reperfusion. Results: The cytokine concentrations in the perfusate were markedly lower with the adsorber, resulting in improved EVLP physiology and biochemistry during the 6-hour perfusion period. Post-transplant dynamic lung compliance was markedly better during the 4-hour reperfusion period in the treatment group. Isolated allograft oxygenation function and dynamic compliance were continued to be superior in the adsorber group at the end of reperfusion accompanied by a markedly decreased local inflammatory response. Conclusions: Implementation of an additional cytokine adsorber has refined the standard EVLP protocol. Furthermore, cytokine removal during EVLP improved immediate post-transplant graft function together with a less intense inflammatory response to reperfusion in pigs. Further studies are warranted to understand the beneficial effects of perfusate adsorption during EVLP in the clinical setting.
Normothermic machine perfusion is clinically used to assess the quality of marginal donor lungs. Although subnormothermic temperatures have proven beneficial for other solid organ transplants, subnormothermia-related benefits of ex vivo lung perfusion (EVLP) still need to be investigated. Material and Methods: In a rat model, we evaluated the effects of 28 °C temperature on 4-h EVLPs with subsequent left lung transplantation. The recipients were observed for 2 h postoperatively. Lung physiology data were recorded and metabolic parameters were assessed. Results: During the 4-h subnormothermic EVLP, the lung oxygenation was significantly higher (p < 0.001), pulmonary vascular resistance (PVR) lower and dynamic compliance (Cdyn) higher when compared to the 37 °C EVLP. During an end-of-EVLP stress test, we recorded significantly higher flow (p < 0.05), lower PVR (p < 0.05) and higher Cdyn (p < 0.01) in the 28 °C group when compared to the 37 °C group. After the left lung transplantation, Cdyn and oxygenation improved in the 28 °C group, which were comparable to the 37 °C group. Chemokines RANTES, MIP-3α, MIP-1α MCP-1 GRO/KC and pro-inflammatory mediators GM-CSF, G-CSF and TNFα were significantly lower after the 28 °C EVLP and remained low in the plasma of the recipient rats after transplantation. The lungs of the 28 °C group showed significantly lowered myeloperoxidase activity and lowered levels of TNFα and IL-1β. Conclusions: Compared to the normothermic perfusion, the 28 °C EVLP improved Cdyn and PVR and reduced both the release of pro-inflammatory cytokines and myeloperoxidase activity in lung tissue. These observations were also observed after the left lung transplantation in the subnormothermic group. The 28 °C EVLP significantly improved biochemical, physiological and inflammatory parameters in lung donors.
Digital monitoring of peak air leakage and patterns of air leakage were useful for predicting prolonged air leak after pulmonary resection. Information on the disappearance of air leak could be derived from the change in the rate of air leakage and from the increase in fluctuation of pleural pressure.
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