37 EFFECT OF THE INTERACTION BETWEEN EXTENDED CRITERIA DONOR VARIABLES AND THE MELD-SCORE ON ISCHEMIA-REPERFUSION INJURY AND PRIMARY GRAFT DYSFUNCTION

2009 ◽  
Vol 50 ◽  
pp. S16
Author(s):  
J. Briceño ◽  
R. Ciria Bru ◽  
M. de la Mata ◽  
S. Rufian ◽  
P. Lopez-Cillero
Keyword(s):  
Reperfusion Injury ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Meld Score ◽  
Primary Graft Dysfunction ◽  
Graft Dysfunction ◽  
Extended Criteria Donor

scholarly journals Minimizing Ischemia Reperfusion Injury in Xenotransplantation

2021 ◽  
Vol 12 ◽  
Author(s):  
Parth M. Patel ◽  
Margaret R. Connolly ◽  
Taylor M. Coe ◽  
Anthony Calhoun ◽  
Franziska Pollok ◽  
...  
Keyword(s):  
Heart Transplantation ◽  
Reperfusion Injury ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Primary Graft Dysfunction ◽  
Graft Dysfunction ◽  
Associated Injury ◽  
Genetic Modifications ◽  
Injury Mechanisms ◽  
Human Primate

The recent dramatic advances in preventing “initial xenograft dysfunction” in pig-to-non-human primate heart transplantation achieved by minimizing ischemia suggests that ischemia reperfusion injury (IRI) plays an important role in cardiac xenotransplantation. Here we review the molecular, cellular, and immune mechanisms that characterize IRI and associated “primary graft dysfunction” in allotransplantation and consider how they correspond with “xeno-associated” injury mechanisms. Based on this analysis, we describe potential genetic modifications as well as novel technical strategies that may minimize IRI for heart and other organ xenografts and which could facilitate safe and effective clinical xenotransplantation.

scholarly journals Biomarkers of Cellular Apoptosis and Necrosis in Donor Myocardium Are Not Predictive of Primary Graft Dysfunction

2016 ◽  
pp. 251-257 ◽  
Author(s):  
O. SZARSZOI ◽  
J. BESIK ◽  
M. SMETANA ◽  
J. MALY ◽  
M. URBAN ◽  
...  
Keyword(s):  
Cell Death ◽  
Prospective Study ◽  
Reperfusion Injury ◽  
Caspase 3 ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Transplant Recipients ◽  
Primary Graft Dysfunction ◽  
Graft Dysfunction ◽  
Apoptosis Markers

Primary graft dysfunction (PGD) is a life-threatening complication among heart transplant recipients and a major cause of early mortality. Although the pathogenesis of PGD is still unclear, ischemia/reperfusion injury has been identified as a predominant factor. Both necrosis and apoptosis contribute to the loss of cardiomyocytes during ischemia/reperfusion injury, and this loss of cells can ultimately lead to PGD. The aim of our prospective study was to find out whether cell death, necrosis and apoptosis markers present in the donor myocardium can predict PGD. The prospective study involved 64 consecutive patients who underwent orthotopic heart transplantation at our institute between September 2010 and January 2013. High-sensitive cardiac troponin T (hs-cTnT) as a marker of minor myocardial necrosis was detected from arterial blood samples before the donor’s pericardium was opened. Apoptosis (caspase-3, active + pro-caspase-3, bcl-2, TUNEL) was assessed from bioptic samples taken from the right ventricle prior graft harvesting. In our study, 14 % of transplant recipients developed PGD classified according to the standardized definition proposed by the ISHLT Working Group. We did not find differences between the groups in regard to hs-cTnT serum levels. The mean hs-cTnT value for the PGD group was 57.4±22.9 ng/l, compared to 68.4±10.8 ng/l in the group without PGD. The presence and severity of apoptosis in grafted hearts did not differ between grafts without PGD and hearts that subsequently developed PGD. In conclusion, our findings did not demonstrate any association between measured myocardial cell death, necrosis or apoptosis markers in donor myocardium and PGD in allograft recipients. More detailed investigations of cell death signaling pathways in transplanted hearts are required.

scholarly journals Primary graft dysfunction of the liver: definitions, diagnostic criteria and risk factors

2016 ◽  
Vol 14 (4) ◽  
pp. 567-572 ◽  
Author(s):  
Douglas Bastos Neves ◽  
Marcela Balbo Rusi ◽  
Luiz Gustavo Guedes Diaz ◽  
Paolo Salvalaggio
Keyword(s):  
Risk Factors ◽  
Liver Transplantation ◽  
Diagnostic Criteria ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Primary Graft Dysfunction ◽  
Graft Dysfunction ◽  
Allograft Dysfunction ◽  
Pubmed Database ◽  
Early Allograft Dysfunction

ABSTRACT Primary graft dysfunction is a multifactorial syndrome with great impact on liver transplantation outcomes. This review article was based on studies published between January 1980 and June 2015 and retrieved from PubMed database using the following search terms: “primary graft dysfunction”, “early allograft dysfunction”, “primary non-function” and “liver transplantation”. Graft dysfunction describes different grades of graft ischemia-reperfusion injury and can manifest as early allograft dysfunction or primary graft non-function, its most severe form. Donor-, surgery- and recipient-related factors have been associated with this syndrome. Primary graft dysfunction definition, diagnostic criteria and risk factors differ between studies.

Use of pulmonoplegia and delivery system during recipient surgery in lung transplantation

Perfusion ◽  
2020 ◽  
Vol 35 (7) ◽  
pp. 587-590
Author(s):  
Brandon C Shade ◽  
Steven Dudley ◽  
Tara McCabe ◽  
Kathryn Gray-DeAngelis
Keyword(s):  
Lung Transplantation ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
The United States ◽  
Primary Graft Dysfunction ◽  
Graft Dysfunction ◽  
Transplant Program ◽  
Heart Lung Machine ◽  
Major Attention ◽  
Lung Machine

Lung transplantation in the United States has steadily grown over the last decade. Major attention has been with the understanding of lung ischemia–reperfusion injury and how it relates to primary graft dysfunction. In 2015, our institution implemented the use of a pulmonoplegia solution during recipient surgery of lung transplantation. A unique circuit utilizing the heart lung machine is used to deliver the pulmonoplegia solution. This system is considered to be a key contributing factor to the success of our lung transplant program.

scholarly journals Endogenous Interleukin-33 Acts as an Alarmin in Liver Ischemia-Reperfusion and Is Associated With Injury After Human Liver Transplantation

2021 ◽  
Vol 12 ◽  
Author(s):  
Louise Barbier ◽  
Aurélie Robin ◽  
Rémy Sindayigaya ◽  
Héloïse Ducousso ◽  
Fanny Dujardin ◽  
...  
Keyword(s):  
Liver Transplantation ◽  
Renal Failure ◽  
Mouse Model ◽  
Reperfusion Injury ◽  
Human Liver ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Graft Dysfunction ◽  
Hepatic Ischemia ◽  
Transplant Patients

Ischemia and reperfusion injury is an early inflammatory process during liver transplantation that impacts on graft function and clinical outcomes. Interleukin (IL)-33 is a danger-associated molecular pattern involved in kidney ischemia/reperfusion injury and several liver diseases. The aims were to assess whether IL-33 was released as an alarmin responsible for ischemia/reperfusion injury in a mouse model of warm hepatic ischemia, and whether this hypothesis could also apply in the setting of human liver transplantation. First, a model of warm hepatic ischemia/reperfusion was used in wild-type and IL-33–deficient mice. Severity of ischemia/reperfusion injury was assessed with ALT and histological analysis. Then, serum IL-33 was measured in a pilot cohort of 40 liver transplant patients. Hemodynamic postreperfusion syndrome, graft dysfunction (assessed by model for early allograft scoring >6), renal failure, and tissue lesions on time-zero biopsies were assessed. In the mouse model, IL-33 was constitutively expressed in the nucleus of endothelial cells, immediately released in response to hepatic pedicle clamping without neosynthesis, and participated in the recruitment of neutrophils and tissue injury on site. The kinetics of IL-33 in liver transplant patients strikingly matched the ones in the animal model, as attested by serum levels reaching a peak immediately after reperfusion, which correlated to clinical outcomes including postreperfusion syndrome, posttransplant renal failure, graft dysfunction, and histological lesions of ischemia/reperfusion injury. IL-33 was an independent factor of graft dysfunction with a cutoff of IL-33 at 73 pg/ml after reperfusion (73% sensitivity, area under the curve of 0.76). Taken together, these findings establish the immediate implication of IL-33 acting as an alarmin in liver I/R injury and provide evidence of its close association with cardinal features of early liver injury-associated disorders in LT patients.

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