We compared the novel normothermic acellular ex vivo liver perfusion (NEVLP) with conventional cold static organ preservation for livers retrieved after cardiac death.

Methods: Pig livers were either subjected to 1hr warm ischemia plus 12hrs cold storage in UW (n=5) or 1hr warm ischemia plus 4hr cold storage plus 8hr NEVLP. After 12hr organ preservation liver transplantation was performed. Liver injury and function was assessed by H&E staining, AST, and bile production. Hepatic energy content was determined by ATP and glycogen levels in biopsies taken before explantation, after warm ischemia and 8 hs after transplantation. Beta galactosidase and TNFΑ were evaluated as marker of Kupffer cell activation.

Results: NEVLP was associated with significantly decreased AST levels (768+547 U/L vs 1640+760 U/L, p<0.01) and less necrosis (10% vs 35%, p<0.05). Cold storage was associated with loss of peripheral arterial blood supply, while arterial blood flow was maintained in NEVLP preserved grafts. Cold stored grafts had massive biliary necrosis (90%), while bile ducts were normal in NEVLP preserved livers. Warm ischemia decreased ATP and glycogen content 10% each. The ATP levels in NEVLP grafts were re-established to baseline levels after transplantation, while glycogen content reached 30% of sham livers. During NEVLP beta-galactosidase activity increased fourfold (from 91ng/ml to 396 ng/ml), while TNFΑ levels tripled (from 401ng/ml to 1500ng/ml).

Conclusion: Acellular NEVLP decreases hepatocyte and bile duct injury in DCD grafts. High beta galactosidase activity and increasing TNF-alpha levels during NEVLP indicate an activation of Kupffer cells. Moreover hepatic glycogen content was decreased. Glycogen restorage and management of Kupffer cell derived inflammation need further investigations.

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