Mechanism of primary graft non-function in a rat model for fatty liver transplantation

K. Hatsugai, N. Ohkohchi, T. Fukumori, Y. Akamatsu, S. Satomi

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13 Citations (Scopus)

Abstract

We established a fatty liver model in rat suitable for the model of human liver with steatosis by cholesterol enriched chow, and investigated the mechanism of primary graft non-function in fatty liver transplantation (LTx) using this model. Grafts with steatosis caused primary graft dysfunction after LTx following even short cold preservation; however, no significant difference was recognized in mitochondrial function of the graft during preservation. Morphological findings were not different at 1 h after reperfusion between non-steatotic and steatotic livers. Focal necrosis of hepatocytes was seen and the sinusoidal endothelial cells were injured 24 h after reperfusion. In addition, the fluidity of the plasma membrane decreased in fatty liver. Our results indicate that deterioration of sinusoidal endothelial cells after reperfusion causes graft dysfunction in LTx of steatotic liver.

Original languageEnglish
Pages (from-to)S583-S590
JournalTransplant International
Volume13
Issue numberSUPPL. 1
Publication statusPublished - 2000 Dec 1

Keywords

  • Cholesterol-rich chow
  • Fatty liver transplantation
  • Mitochondrial function
  • Plasma membrane
  • Primary graft non-function
  • Sinusoidal endothelial cell

ASJC Scopus subject areas

  • Transplantation

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  • Cite this

    Hatsugai, K., Ohkohchi, N., Fukumori, T., Akamatsu, Y., & Satomi, S. (2000). Mechanism of primary graft non-function in a rat model for fatty liver transplantation. Transplant International, 13(SUPPL. 1), S583-S590.