Inactivation of Kupffer cells after prolonged donor fasting improves viability of transplanted hepatic allografts.

Abstract

Data from recent studies suggest that donor fasting imparts a beneficial effect on the viability of transplanted hepatic allografts. Because starvation may temporarily inactivate Kupffer cells, and because these cells are the likely mediators of liver injury after prolonged preservation-reperfusion, the purpose of this study is to establish a link between improved organ viability and Kupffer cell inactivation caused by donor allograft fasting. In an in vivo rat liver transplant model, 48 hours of donor fasting (1) improved allograft viability, (2) significantly decreased Kupffer cell phagocytosis, and (3) significantly decreased cytokine (tumor necrosis factor [TNF]) production postrevascularization. These data validate work from previous studies demonstrating that donor fasting improves allograft viability and furthermore support our previous research implicating activation of Kupffer cells as a causative agent of cold ischemia-preservation injury.

• Authors: H N Sankary, A Chong, P Foster, E Brown, J Shen, R Kimura, G Rayudu, J Williams
• Journal: Hepatology (Baltimore, Md.) (Hepatology) Vol. 22 Issue 4 Pt 1 Pg. 1236-42 (Oct 1995) ISSN: 0270-9139 [Print] United States
• PMID: 7557876 (Publication Type: Journal Article)

Chemical References

• Tumor Necrosis Factor-alpha
• Technetium Tc 99m Sulfur Colloid

Topics

• Animals
• Fasting
• Graft Survival
• Kupffer Cells (physiology)
• Liver (blood supply, metabolism)
• Liver Transplantation
• Phagocytosis
• Rats
• Rats, Inbred Lew
• Technetium Tc 99m Sulfur Colloid (metabolism)
• Tissue Donors
• Tumor Necrosis Factor-alpha (biosynthesis)