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Postmortem normothermic regional perfusion (NRP) is a rising preservation strategy in controlled donation after circulatory determination of death (cDCD). Herein, we present results for cDCD liver transplants performed in Spain 2012–2019, with outcomes evaluated through December 31, 2020. Results were analyzed retrospectively and according to recovery technique (abdominal NRP [A‐NRP] or standard rapid recovery [SRR]). During the study period, 545 cDCD liver transplants were performed with A‐NRP and 258 with SRR. Median donor age was 59 years (interquartile range 49–67 years). Adjusted risk estimates were improved with A‐NRP for overall biliary complications (OR 0.300, 95% CI 0.197–0.459, p < .001), ischemic type biliary lesions (OR 0.112, 95% CI 0.042–0.299, p < .001), graft loss (HR 0.371, 95% CI 0.267–0.516, p < .001), and patient death (HR 0.540, 95% CI 0.373–0.781, p = .001). Cold ischemia time (HR 1.004, 95% CI 1.001–1.007, p = .021) and re‐transplantation indication (HR 9.552, 95% CI 3.519–25.930, p < .001) were significant independent predictors for graft loss among cDCD livers with A‐NRP. While use of A‐NRP helps overcome traditional limitations in cDCD liver transplantation, opportunity for improvement remains for cases with prolonged cold ischemia and/or technically complex recipients, indicating a potential role for complimentary ex situ perfusion preservation techniques.

Poly(ADP-ribose) polymerase-1 (PARP-1) has been involved in endothelial cell dysfunction associated with various pathophysiological conditions. The intrinsic mechanism of PARP-1-mediated endothelial cell dysfunction could be related to PARP-1 overactivation, NAD(+) consumption and ATP depletion. An alternative way could involve transcription regulation. By using high-density microarrays, we examined early tumor necrosis factor alpha (TNF-alpha)-stimulated gene expression profiles in PARP-1(+/+) and PARP-1(-/-) murine heart endothelial cells. TNF-alpha modulated a significant number of genes in both cell types. We have identified a set of genes whose expression in response to TNF-alpha is modulated by PARP-1, whereas the expression of others is PARP-1-independent. Up-regulation of several genes involved in the inflammatory response is hampered in the absence of PARP-1. Moreover, NF-kappaB-dependent transcriptional activation is partially inhibited in PARP-1(-/-) compared to PARP-1(+/+) cells. However, we found that PARP-1 might also silence transcription of several NF-kappaB target genes. Overall, our results show that PARP-1 is regulating the expression of genes by the endothelial cells both in a positive and a negative fashion, with the final effects depending on the gene. Individual studies of these genes are now necessary to clarify the intrinsic mechanism by which PARP-1 is controlling transcription and thereby finding out different therapeutic approaches involving PARP-1.

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