Spannbauer M M, Oleszczuk A, Tannapfel A, Blüher M, Pietsch U C, Hengstler J, Donaubauer B, Madaj-Sterba P, Fürll M, Schuhmacher A, Thiery J, Hauss J P, Schön M R
Department of Surgery, Charité, Humboldt-University, Berlin, Germany.
Transplant Proc. 2005 Jan-Feb;37(1):210-1. doi: 10.1016/j.transproceed.2004.12.136.
Steatotic liver grafts are associated with a high incidence of primary nonfunction and initial poor function. Due to the increasing number of liver transplant candidates, centers are inclined to accept marginal donors more frequently. For a lack of a reliable fatty liver model, preservation concepts for fatty livers have hardly been evaluated. Moreover, there is an ongoing debate on the relevance and impact of micro- versus macrovesicular steatotic organs. We therefore intended to establish a steatotic liver model in pigs comprising both micro- and macrovesicular steatotic livers. Five groups of pigs received daily 1 to 6 g ethanol/kg body weight and/or a protein-deficient diet for up to 72 days. Liver biopsy was carried out at days 24, 48, and 72. With an increasing amount and duration of ethanol intake, higher levels of microvesicular steatosis were induced. Ethanol and protein deficient diet resulted in more than 60% microvesicular steatosis after 72 days. Exclusively protein-deficient diet without ethanol induced macrovesicular steatosis of more than 70% after 72 days. For the first time, we established a porcine model of hepatic steatosis that comprises both histologic types of fatty liver: micro- and macrovesicular steatosis induced by ethanol and a protein-deficient diet. We would like to conclude that our model is particularly qualified to study new concepts of preservation for steatotic livers to improve on the posttransplant outcome.
脂肪变性的肝脏移植物与原发性无功能和初始功能不良的高发生率相关。由于肝移植候选者数量的增加，各中心更倾向于更频繁地接受边缘供体。由于缺乏可靠的脂肪肝模型，脂肪性肝脏的保存概念几乎未得到评估。此外，关于微泡性与大泡性脂肪变性器官的相关性和影响的争论仍在继续。因此，我们打算在猪身上建立一个同时包含微泡性和大泡性脂肪变性肝脏的脂肪肝模型。五组猪每天接受1至6克乙醇/千克体重和/或蛋白质缺乏饮食，持续72天。在第24、48和72天进行肝脏活检。随着乙醇摄入量和摄入持续时间的增加，诱导出更高水平的微泡性脂肪变性。乙醇和蛋白质缺乏饮食在72天后导致超过60%的微泡性脂肪变性。仅蛋白质缺乏饮食而无乙醇在72天后诱导出超过70%的大泡性脂肪变性。我们首次建立了一种肝脂肪变性的猪模型，该模型包含两种组织学类型的脂肪肝：由乙醇和蛋白质缺乏饮食诱导的微泡性和大泡性脂肪变性。我们可以得出结论，我们的模型特别适合研究脂肪性肝脏保存的新概念，以改善移植后的结果。
