ArticleThe Journal of heart and lung transplantation : the official publication of the International Society for Heart Transplantation2016
The relationship between plasma lipid peroxidation products and primary graft dysfunction after lung transplantation is modified by donor smoking and reperfusion hyperoxia.
Article in The Journal of heart and lung transplantation : the official publication of the International Society for Heart Transplantation, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 30 citations in OpenAlex.
- The prognostic role of preoperative subcutaneous adipose tissue measurement in lung transplantation.BMC pulmonary medicine · 2026Article
- Primary graft dysfunction following lung transplantation: From pathogenesis to future frontiers.World journal of transplantation · 2023Review
- Cigarette Smoke Exposure and Acute Respiratory Distress Syndrome in Sepsis: Epidemiology, Clinical Features, and Biologic Markers.American journal of respiratory and critical care medicine · 2022Article
- Volatile organic compound profiling to explore primary graft dysfunction after lung transplantation.Scientific reports · 2022Article
- Risk of primary graft dysfunction following lung transplantation in selected adults with connective tissue disease-associated interstitial lung disease.The Journal of heart and lung transplantation : the official publication of the International Society for Heart Transplantation · 2021Article
- Adipose tissue quantification and primary graft dysfunction after lung transplantation: The Lung Transplant Body Composition study.The Journal of heart and lung transplantation : the official publication of the International Society for Heart Transplantation · 2019Article
- Aryl-Hydrocarbon Receptor Repressor Gene in Primary Graft Dysfunction after Lung Transplantation.American journal of respiratory cell and molecular biology · 2019Article
- The Future of Lung Transplantation.Chest · 2019Review
- Cell-free hemoglobin promotes primary graft dysfunction through oxidative lung endothelial injury.JCI insight · 2018Article
- Lipid (per) oxidation in mitochondria: an emerging target in the ageing process?Biogerontology · 2017Review
- Clinical Risk Factors and Prognostic Model for Primary Graft Dysfunction after Lung Transplantation in Patients with Pulmonary Hypertension.Annals of the American Thoracic Society · 2017Article
- Primary graft dysfunction: pathophysiology to guide new preventive therapies.Expert review of respiratory medicine · 2017Review
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Authors and funding
27 authors at 13 institutions in 1 country.
Funding
Abstract
backgroundDonor smoking history and higher fraction of inspired oxygen (FIO2) at reperfusion are associated with primary graft dysfunction (PGD) after lung transplantation. We hypothesized that oxidative injury biomarkers would be elevated in PGD, with higher levels associated with donor exposure to cigarette smoke and recipient hyperoxia at reperfusion.
methodsWe performed a nested case-control study of 72 lung transplant recipients from the Lung Transplant Outcomes Group cohort. Using mass spectroscopy, F2-isoprostanes and isofurans were measured in plasma collected after transplantation. Cases were defined in 2 ways: grade 3 PGD present at day 2 or day 3 after reperfusion (severe PGD) or any grade 3 PGD (any PGD).
resultsThere were 31 severe PGD cases with 41 controls and 35 any PGD cases with 37 controls. Plasma F2-isoprostane levels were higher in severe PGD cases compared with controls (28.6 pg/ml vs 19.8 pg/ml, p = 0.03). Plasma F2-isoprostane levels were higher in severe PGD cases compared with controls (29.6 pg/ml vs 19.0 pg/ml, p = 0.03) among patients reperfused with FIO2 >40%. Among recipients of lungs from donors with smoke exposure, plasma F2-isoprostane (38.2 pg/ml vs 22.5 pg/ml, p = 0.046) and isofuran (66.9 pg/ml vs 34.6 pg/ml, p = 0.046) levels were higher in severe PGD compared with control subjects.
conclusionsPlasma levels of lipid peroxidation products are higher in patients with severe PGD, in recipients of lungs from donors with smoke exposure, and in recipients exposed to higher Fio2 at reperfusion. Oxidative injury is an important mechanism of PGD and may be magnified by donor exposure to cigarette smoke and hyperoxia at reperfusion.
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