Liver Regeneration Induced By Extracorporeal Portal Vein Arterialization in a Swine Model of Carbon Tetrachloride Intoxication.

Transplant Proc

Center for Applied Biomedical Research, S. Orsola-Malpighi University Hospital Bologna, Bologna, Italy; Department of Medicine and Surgical Sciences, University of Bologna, Bologna, Italy. Electronic address:

Published: September 2015

Introduction: This study aimed to determine whether a controlled portal blood arterialization by a liver extracorporeal device (L.E.O2 NARDO) is effective in treating acute hepatic failure (AHF) induced in swine by carbon tetrachloride (CCl4) administration.

Materials And Methods: Sixteen swine with AHF induced by intraperitoneal injection of CCl4 in oil solution were randomly divided into 2 groups: animals that received L.E.O2 NARDO treatment 48 hours after the intoxication (study group; n = 8); and animals that were sham operated 48 hours after the intoxication (control group; n = 8). Blood was withdrawn from the iliac artery and reversed in the portal venous system by an interposed extracorporeal device. Each treatment lasted 6 hours. The survival was assessed at 5 days after L.E.O2 NARDO treatment or sham operation. In both groups blood samples were collected for biochemical analysis at different study time and liver biopsies were performed 48 hours after intoxication and at humane killing.

Results: In the study group decreased transaminases levels and a more rapid international normalized ratio (INR) recover were detected as compared with the control group. Six animals of the study group (75%) versus 1 animal (12.5%) of the control group survived at 5 days after surgery with a statistically significant difference (P < .05). Liver biopsies performed at humane killing showed damaged areas of the livers reduced in the study group compared with biopsies of the control group.

Conclusions: Arterial blood supply in the portal system through the L.E.O2 NARDO device is easily applicable, efficacious, and safe in a swine model of AHF induced by CCl4 intoxication.

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http://dx.doi.org/10.1016/j.transproceed.2014.11.079DOI Listing

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