Argon and xenon ventilation during prolonged ex vivo lung perfusion

Martens, A; Montoli, M.; Faggi, Giulio; Katz, Ira; Pype, J L; Vanaudenaerde, Bart M.; Raemdonck, Dirk Van; Neyrinck, Arne

doi:10.1016/j.jss.2015.10.007

Cited by 26 publications

(31 citation statements)

References 63 publications

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“…To allow for perconditioning, the lungs were exposed to Ar during cold preservation by inflation with the same gas mixture used as during the preconditioning phase (FiO 2 21% with 79% N 2 or Ar). The postconditioning phase during EVLP was optimized compared to the previous postconditioning protocol 7. Indeed: the oxygen concentration in the gas mixture of the ventilator was lowered to 12% instead of 21% to allow for a higher Ar concentration of 88% (or 88% N 2 in the CONTR group).…”

Section: Discussionmentioning

confidence: 99%

“…Our previous study, which investigated a postconditioning effect of argon (Ar) (and xenon (Xe)) on pulmonary ischemia-reperfusion injury, could not confirm such a positive reconditioning effect in lungs7; despite the fact that beneficial postconditioning effects of Ar have been shown in other injury models such as cardiac arrest,89 brain injury,10 and neonatal asphyxia 11. The noble gases Ar and Xe have also previously been investigated as a reconditioning strategy in IRI kidney transplant models showing beneficial effects on graft function 1213.…”

Section: Introductionmentioning

confidence: 91%

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A porcine ex vivo lung perfusion model with maximal argon exposure to attenuate ischemia-reperfusion injury

et al. 2017

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Argon (Ar) is a noble gas with known organoprotective effects in rodents and in vitro models. In a previous study we failed to find a postconditioning effect of Ar during ex vivo lung perfusion (EVLP) on warm-ischemic injury in a porcine model. In this study, we further investigated a prolonged exposure to Ar to decrease cold ischemia-reperfusion injury after lung transplantation in a porcine model with EVLP assessment. Domestic pigs (n = 6/group) were pre-conditioned for 6 hours with 21% O2 and 79% N2 (CONTR) or 79% Ar (ARG). Subsequently, lungs were cold flushed and stored inflated on ice for 18 hours inflated with the same gas mixtures. Next, lungs were perfused for 4 hours on EVLP (acellular) while ventilated with 12% O2 and 88% N2 (CONTR group) or 88% Ar (ARG group). The perfusate was saturated with the same gas mixture but with the addition of CO2 to an end-tidal CO2 of 35-45 mmHg. The saturated perfusate was drained and lungs were perfused with whole blood for an additional 2 hours on EVLP. Evaluation at the end of EVLP did not show significant effects on physiologic parameters by prolonged exposure to Ar. Also wet-to-dry weight ratio did not improve in the ARG group. Although in other organ systems protective effects of Ar have been shown, we did not detect beneficial effects of a high concentration of Ar on cold pulmonary ischemia-reperfusion injury in a porcine lung model after prolonged exposure to Ar in this porcine model with EVLP assessment.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 91%

A porcine ex vivo lung perfusion model with maximal argon exposure to attenuate ischemia-reperfusion injury

et al. 2017

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“…The production of the perfusate and technique of EVLP are performed as described previously [27]. After a 1-hour rewarming period and slow increase of the flow to 40% of the estimated cardiac output (calculated as 100 ml/kg) lungs were further perfused and evaluated for 6 hours in total.…”

Section: Methodsmentioning

confidence: 99%

Immunoregulatory effects of multipotent adult progenitor cells in a porcine ex vivo lung perfusion model

et al. 2017

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BackgroundPrimary graft dysfunction (PGD) is considered to be the end result of an inflammatory response targeting the new lung allograft after transplant. Previous research has indicated that MAPC cell therapy might attenuate this injury by its paracrine effects on the pro-/anti-inflammatory balance. This study aims to investigate the immunoregulatory capacities of MAPC cells in PGD when administered in the airways.MethodsLungs of domestic pigs (n = 6/group) were subjected to 90 minutes of warm ischemia. Lungs were cold flushed, cannulated on ice and placed on EVLP for 6 hours. At the start of EVLP, 40 ml of an albumin-plasmalyte mixture was distributed in the airways (CONTR group). In the MAPC cell group, 150 million MAPC cells (ReGenesys/Athersys, Cleveland, OH, USA) were added to this mixture. At the end of EVLP, a physiological evaluation (pulmonary vascular resistance, lung compliance, PaO2/FiO2), wet-to-dry weight ratio (W/D) sampling and a multiplex analysis of bronchoalveolar lavage (BAL) (2 × 30 ml) was performed.ResultsPulmonary vascular resistance, lung compliance, PaO2/FiO2 and W/D were not statistically different at the end of EVLP between both groups. BAL neutrophilia was significantly reduced in the MAPC cell group. Moreover, there was a significant decrease in TNF-α, IL-1β and IFN-γ in the BAL, but not in IFN-α; whereas IL-4, IL-10 and IL-8 were below the detection limit.ConclusionsAlthough no physiologic effect of MAPC cell distribution in the airways was detected during EVLP, we observed a reduction in pro-inflammatory cytokines and neutrophils in BAL in the MAPC cell group. This effect on the innate immune system might play an important role in critically modifying the process of PGD after transplantation. Further experiments will have to elucidate the immunoregulatory effect of MAPC cell administration on graft function after transplantation.

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“…These gases can also be added to the gas mixture used during EVLP (92). Attenuation of organ damage following ischemia and reperfusion has been attributed to an increase in apoptosis, an increase in HIF1-alpha or modification of the Aktpathway (93).…”

Section: Noble Gasesmentioning

confidence: 99%

“…Attenuation of organ damage following ischemia and reperfusion has been attributed to an increase in apoptosis, an increase in HIF1-alpha or modification of the Aktpathway (93). However, not all evidence supports this possibly beneficial role (92). There is still a lack of evidence concerning the pathways that are involved in the protective effect of these noble gases, and timing of administration and correct dosage are still uncertain.…”

Section: Noble Gasesmentioning

confidence: 99%

Oxidative and nitrosative stress during pulmonary ischemia-reperfusion injury: from the lab to the OR

Gielis¹,

Beckers²,

Briedé³

et al. 2017

Ann. Transl. Med.

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Oxidative and nitrosative stress are an umbrella term for pathophysiological processes that involve free radical generation during inflammation. In this review, the involvement of reactive oxygen and nitrogen species is evaluated during lung ischemia-reperfusion injury (LIRI) from a surgical point of view. The main biochemical and cellular mechanisms behind free radical generation are discussed, together with surgical procedures that may cause reperfusion injury. Finally, different therapeutic strategies are further explored. A literature search was performed, searching for "lung ischemia reperfusion injury", "reperfusion injury", "large animal model" and different search terms for each section: "surgery", "treatment", "cellular mechanism", or "enzyme". Although reperfusion injury is not an uncommon entity and there is a lot of evidence concerning myocardial ischemia-reperfusion injury, in the lung this phenomenon is less extensively described and studies in large animals are not easy to come by. With increasing number of patients on waiting lists for lung transplant, awareness for this entity should all but rise.

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Argon and xenon ventilation during prolonged ex vivo lung perfusion

Cited by 26 publications

References 63 publications

A porcine ex vivo lung perfusion model with maximal argon exposure to attenuate ischemia-reperfusion injury

A porcine ex vivo lung perfusion model with maximal argon exposure to attenuate ischemia-reperfusion injury

Immunoregulatory effects of multipotent adult progenitor cells in a porcine ex vivo lung perfusion model

Oxidative and nitrosative stress during pulmonary ischemia-reperfusion injury: from the lab to the OR

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