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Inactivation of kupffer cells after prolonged donor fasting improves viability of transplanted hepatic allografts
Author(s) -
Sankary Howard N.,
Chong Anita,
Foster Preston,
Brown Esther,
Shen Jikun,
Kimura Robert,
Rayudu Guarimella,
Williams James
Publication year - 1995
Publication title -
hepatology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 5.488
H-Index - 361
eISSN - 1527-3350
pISSN - 0270-9139
DOI - 10.1002/hep.1840220432
Subject(s) - kupffer cell , viability assay , hepatology , viaspan , medicine , tumor necrosis factor alpha , in vivo , cytokine , liver transplantation , transplantation , reperfusion injury , endocrinology , immunology , andrology , cell , ischemia , biology , biochemistry , microbiology and biotechnology
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. (H EPATOLOGY 1995; 22:1236–1242.).