Primary Graft Dysfunction After Lung Transplantation

Porteous, Mary K.; Lee, James C.

doi:10.1016/j.ccm.2017.07.005

Cited by 69 publications

(67 citation statements)

References 168 publications

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“…Primary graft dysfunction (PGD) is a form of acute lung injury that is characterized by hypoxemia, pulmonary edema, and lung inflammation that develops within the first 72 hours after lung transplantation (1,2). PGD is the most common cause of short-term mortality after lung transplantation and also conPrimary graft dysfunction (PGD) is acute lung injury within 72 hours of lung transplantation.…”

Section: Introductionmentioning

confidence: 99%

“…tributes to the development of chronic lung allograft dysfunction (2). A variety of clinical risk factors for PGD have been identified with contributions from the donor (3)(4)(5)(6)(7), the recipient (3)(4)(5)(7)(8)(9)(10), and operative variables (4,5,8,11).…”

Section: Introductionmentioning

confidence: 99%

“…A variety of clinical risk factors for PGD have been identified with contributions from the donor (3)(4)(5)(6)(7), the recipient (3)(4)(5)(7)(8)(9)(10), and operative variables (4,5,8,11). In addition, a number of biomarkers have been associated with increased risk of PGD, including markers of innate and adaptive immune activation, epithelial and endothelial injury, coagulation, vascular permeability, and lipid peroxidation (2,(12)(13)(14)(15)(16)(17)(18)(19)(20)(21)(22)(23)(24)(25)(26)(27). Despite identification of these clinical and biomarker predictors of PGD, the mechanisms leading to PGD are not well understood, and there are no specific therapeutic interventions for PGD.…”

Section: Introductionmentioning

confidence: 99%

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Cell-free hemoglobin promotes primary graft dysfunction through oxidative lung endothelial injury

et al. 2018

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Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Cell-free hemoglobin promotes primary graft dysfunction through oxidative lung endothelial injury

et al. 2018

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“…Immune activation plays a major role in lung IR and the development of PGD . It depends primarily on the activation of NF‐κB, which can already occur during EVLP .…”

Section: Discussionmentioning

confidence: 99%

Treatment with 3-aminobenzamide during ex vivo lung perfusion of damaged rat lungs reduces graft injury and dysfunction after transplantation

Wang

Parapanov

Debonneville

et al. 2020

American Journal of Transplantation

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Ex vivo lung perfusion (EVLP) with pharmacological reconditioning may increase donor lung utilization for transplantation (LTx). 3‐Aminobenzamide (3‐AB), an inhibitor of poly(ADP‐ribose) polymerase (PARP), reduces ex vivo lung injury in rat lungs damaged by warm ischemia (WI). Here we determined the effects of 3‐AB reconditioning on graft outcome after LTx. Three groups of donor lungs were studied: Control (Ctrl): 1 hour WI + 3 hours cold ischemia (CI) + LTx; EVLP: 1 hour WI + 3 hours EVLP + LTx; EVLP + 3‐AB: 1 hour WI + 3 hours EVLP + 3‐AB (1 mg.mL−1) + LTx. Two hours after LTx, we determined lung graft compliance, edema, histology, neutrophil counts in bronchoalveolar lavage (BAL), mRNA levels of adhesion molecules within the graft, as well as concentrations of interleukin‐6 and 10 (IL‐6, IL‐10) in BAL and plasma. 3‐AB reconditioning during EVLP improved compliance and reduced lung edema, neutrophil infiltration, and the expression of adhesion molecules within the transplanted lungs. 3‐AB also attenuated the IL‐6/IL‐10 ratio in BAL and plasma, supporting an improved balance between pro‐ and anti‐inflammatory mediators. Thus, 3‐AB reconditioning during EVLP of rat lung grafts damaged by WI markedly reduces inflammation, edema, and physiological deterioration after LTx, supporting the use of PARP inhibitors for the rehabilitation of damaged lungs during EVLP.

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“…During some thoracic surgical procedures, the lung experiences ischaemia/reperfusion (I/R)-induced damage, which, in lung transplants, has been identified as one of the main causes of primary graft failure [1]. I/R injury (IRI) has an important inflammatory component.…”

Section: Introductionmentioning

confidence: 99%

Glycocalyx Degradation after Pulmonary Transplantation Surgery

et al. 2018

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Purpose: Ischaemia-reperfusion injury (IRI) is a main cause of morbidity after pulmonary resection surgery. The degradation of glycocalyx, a dynamic layer of macromolecules at the luminal surface of the endothelium, seems to participate in tissue dysfunction after IRI. Lidocaine has a proven anti-inflammatory activity in several tissues but its modulation of glycocalyx has not been investigated. This work aimed to investigate the potential involvement of glycocalyx in lung IRI in a lung auto-transplantation model and the possible effect of lidocaine in modulating IRI. Methods: Three groups (sham-operated, control, and lidocaine), each consisting of 6 Large White pigs, were subjected to lung auto-transplantation. All groups received the same anaesthesia. In addition, the lidocaine group received a continuous IV administration of lidocaine (1.5 mg/kg/h). Lung tissue and plasma samples were taken before pulmonary artery clamp, before reperfusion, and 30 and 60 min post-reperfusion in order to analyse pulmonary oedema, glycocalyx components, adhesion molecules, and myeloperoxidase level. Results: Ischaemia caused pulmonary oedema, which was greater after reperfusion. This effect was accompanied by decreased levels of syndecan-1 and heparan sulphate in the lung samples, together with increased levels of both glycocalyx components in the plasma samples. After reperfusion, neutrophil activation and the expression of adhesion molecules were increased. All these alterations were significantly lower or absent in the lidocaine group. Conclusion: Lung IRI caused glycocalyx degradation that contributed to neutrophil activation and adhesion. The administration of lidocaine was able to protect the lung from glycocalyx degradation.

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Primary Graft Dysfunction After Lung Transplantation

Cited by 69 publications

References 168 publications

Cell-free hemoglobin promotes primary graft dysfunction through oxidative lung endothelial injury

Cell-free hemoglobin promotes primary graft dysfunction through oxidative lung endothelial injury

Treatment with 3-aminobenzamide during ex vivo lung perfusion of damaged rat lungs reduces graft injury and dysfunction after transplantation

Glycocalyx Degradation after Pulmonary Transplantation Surgery

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