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Clinical Trial
. 2019 Aug 15;14(8):e0221010.
doi: 10.1371/journal.pone.0221010. eCollection 2019.

Graft glycocalyx degradation in human liver transplantation

Arie Passov  1 , Alexey Schramko  1 , Heikki Mäkisalo  2 , Arno Nordin  2 , Sture Andersson  3 , Eero Pesonen  1 , Minna Ilmakunnas  1
Affiliations
Clinical Trial

Graft glycocalyx degradation in human liver transplantation

Arie Passov et al. PLoS One. .

Abstract

Objective: Ischaemia/reperfusion-injury degrades endothelial glycocalyx. Graft glycocalyx degradation was studied in human liver transplantation.

Methods: To assess changes within the graft, blood was drawn from portal and hepatic veins in addition to systemic samples in 10 patients. Plasma syndecan-1, heparan sulfate and chondroitin sulfate, were measured with enzyme-linked immunosorbent assay.

Results: During reperfusion, syndecan-1 levels were higher in graft caval effluent [3118 (934-6141) ng/ml, P = 0.005] than in portal venous blood [101 (75-121) ng/ml], indicating syndecan-1 release from the graft. Concomitantly, heparan sulfate levels were lower in graft caval effluent [96 (32-129) ng/ml, P = 0.037] than in portal venous blood [112 (98-128) ng/ml], indicating heparan sulfate uptake within the graft. Chondroitin sulfate levels were equal in portal and hepatic venous blood. After reperfusion arterial syndecan-1 levels increased 17-fold (P < 0.001) and heparan sulfate decreased to a third (P < 0.001) towards the end of surgery.

Conclusion: Syndecan-1 washout from the liver indicates extensive glycocalyx degradation within the graft during reperfusion. Surprisingly, heparan sulfate was taken up by the graft during reperfusion. Corroborating previous experimental reports, this suggests that endogenous heparan sulfate might be utilized within the graft in the repair of damaged glycocalyx.

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Conflict of interest statement

The authors have declared that no competing interests exist.

Figures

Fig 1
Fig 1. Systemic concentrations of syndecan-1, heparan sulfate and chondroitin sulfate preoperatively (1), before reperfusion (2), 5 min after portal vein declamping (3), and 5 min after hepatic artery declamping (4).
Data are depicted as median and interquartile range. ** P < 0.01 for vs preoperatively (1) and ## P < 0.01 for vs before reperfusion (2) (Wilcoxon Signed Rank test).
Fig 2
Fig 2. Transhepatic gradients [(caval effluent or hepatic vein)–(portal vein)] of syndecan-1, heparan sulfate and chondroitin sulfate at reperfusion (2), 5 minutes after portal vein declamping (3) and 5 minutes after hepatic artery declamping (4).
* P < 0.05 and ** P < 0.01 for hepatic vs portal vein (Wilcoxon Signed Rank test).
See this image and copyright information in PMC

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