Platelet Transfusion During Liver Transplantation Is Associated with Increased Postoperative Mortality Due to Acute Lung Injury

Objective. This study aimed to investigate whether propofol pretreatment can protect against liver transplantation-induced acute lung injury (ALI) and to explore whether Nrf2 pathway is involved in the protections provided by propofol pretreatment.Method. Adult male Sprague-Dawley rats were divided into five groups based on the random number table. Lung pathology was observed by optical microscopy. Lung water content was assessed by wet/dry ratio, and PaO2was detected by blood gas analysis. The contents of H2O2, MDA, and SOD activity were determined by ELISA method, and the expression of HO-1, NQO1, Keap1, and nuclear Nrf2 was assayed by western blotting.Results. Compared with saline-treated model group, both propofol and N-acetylcysteine pretreatment can reduce the acute lung injury caused by orthotopic autologous liver transplantation (OALT), decrease the lung injury scores, lung water content, and H2O2and MDA levels, and improve the arterial PaO2and SOD activity. Furthermore, propofol (but not N-acetylcysteine) pretreatment especially in high dose inhibited the expression of Keap1 and induced translocation of Nrf2 into the nucleus to further upregulate the expression of HO-1 and NQO1 downstream.Conclusion. Pretreatment with propofol is associated with attenuation of OALT-induced ALI, and the Nrf2 pathway is involved in the antioxidative processes.

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Transfusion-related acute lung injury (TRALI) following platelet transfusion in a patient receiving high-dose interleukin-2 for treatment of metastatic renal cell carcinoma

Transfusion and Apheresis Science ◽

10.1016/s1473-0502(03)00094-6 ◽

2003 ◽

Vol 29 (1) ◽

pp. 25-27 ◽

Cited By ~ 16

Author(s):

Bruno C. Medeiros ◽

Karen E. Kogel ◽

Madeleine A Kane

Keyword(s):

Renal Cell Carcinoma ◽

Acute Lung Injury ◽

Lung Injury ◽

Cell Carcinoma ◽

Metastatic Renal Cell Carcinoma ◽

Renal Cell ◽

Platelet Transfusion ◽

Interleukin 2 ◽

High Dose

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Intraoperative use of low volume ventilation to decrease postoperative mortality, mechanical ventilation, lengths of stay and lung injury in patients without acute lung injury

10.1002/14651858.cd011151 ◽

2014 ◽

Cited By ~ 2

Author(s):

Dat-Nhut Nguyen ◽

Joanne Guay ◽

Edward A Ochroch

Keyword(s):

Mechanical Ventilation ◽

Acute Lung Injury ◽

Lung Injury ◽

Postoperative Mortality ◽

Lengths Of Stay ◽

Volume Ventilation ◽

Low Volume

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Stabilizing mast cells improves acute lung injury after orthotopic liver transplantation via promotion of apoptosis in polymorphonuclear neutrophils

AJP Lung Cellular and Molecular Physiology ◽

10.1152/ajplung.00046.2020 ◽

2020 ◽

Author(s):

Chaojin Chen ◽

Zheng Zhang ◽

Fang Tan ◽

Fanbing Meng ◽

Lifei Lai ◽

...

Keyword(s):

Liver Transplantation ◽

Acute Lung Injury ◽

Mast Cells ◽

Lung Injury ◽

Orthotopic Liver Transplantation ◽

Inflammatory Cells ◽

Pulmonary Complications ◽

Polymorphonuclear Neutrophils ◽

Inflammatory Factor ◽

Tnf Α

Aims: Postoperative pulmonary complications including acute lung injury (ALI) and acute respiratory distress syndrome have contributed to the mortality and morbidity of orthotopic liver transplantation (OLT) with unclear mechanisms. Mast cells (MCs) and polymorphonuclear neutrophils (PMNs) are the main inflammatory cells and participants in the process of ALI. The present study was designed to investigate the role of MCs and PMNs and their potential relation to ALI following OLT. Main Methods: Rat orthotopic autologous liver transplantation (OALT) model was designed to determine lung injury at different time points after liver reperfusion. We also evaluated the function of MCs and the effect of TNF-α and tryptase on ALI and PMN apoptosis in rats subjected to OALT. Histological scores and inflammatory factor levels as well as PMN apoptosis were measured. Key findings: Rats suffered from ALI after OALT, which was demonstrated with collapse of pulmonary architecture, pulmonary edema, and infiltration of inflammatory cells in alveolar and interstitial spaces, as well as increased levels of pro-inflammatory cytokines. ALI maximized at 8 h after OALT. However, PMN apoptosis lagged behind the pulmonary injury and maximized at 16 h after OALT, when the acute inflammation resolution initiated. MC stabilization, and tryptase and TNF-α inhibitors could significantly decrease the lung pathophysiologic scores accompanied with an increase in PMN apoptosis. Significance: ALI after OLT was associated with MC activation and PMN apoptosis. The ALI progression might be affected by delayed PMN apoptosis, which was related to MC activation. Induction of PMN apoptosis might alleviate ALI after OALT.

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