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

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

研究成果: Article

13 引用 (Scopus)

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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.

元の言語English
ページ(範囲)S583-S590
ジャーナルTransplant International
13
発行部数SUPPL. 1
出版物ステータスPublished - 2000 12 1

ASJC Scopus subject areas

  • Transplantation

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  • これを引用

    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.