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. 2020 Dec 1;10:20966. doi: 10.1038/s41598-020-77915-0

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© The Author(s) 2020

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/.

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Injury markers and liver function in experimental groups. Arterial PV group blue circles, n = 5 experiments, venous PV group red triangles, n = 5 experiments. (a–c) Injury marker release in perfusate shown for AST (a), cytochrome c (b) and 8-OHdG (c). (d,e) Representative staining showing integrity on H&E staining (g) and preserved glycogen stores in PAS staining (h) after one week of perfusion. (f) Representative immunohistochemistry staining for Caspase 3 showing absence of relevant apoptosis on perfusion day 7. (d) Macrophages were not activated in both groups as shown with TLR4 at mRNA level. (e) Endothelial cell activation at mRNA level expressed with ICAM-1. (i) similarly to ICAM-1, von Willebrand Factor immunohistochemistry staining showed absence of relevant endothelial cell activation. (j) Bile flow was constantly present in both experimental groups for one week. (k,l) Livers cleared lactate (k) and maintained albumin level (l) in perfusate. P value * < 0.05, ** < 0.01, *** < 0.001. ns not significant.