Heijnen Bob H M, Straatsburg Irene H, Gouma Dirk J, van Gulik Thomas M
Surgical laboratory, IWO 10151, Academic Medical Center, Meibergdreef 9, 1105 AZ Amsterdam, The Netherlands.
Surgery. 2003 Nov;134(5):806-17. doi: 10.1016/s0039-6060(03)00125-9.
We attempted to assess liver ischemia/reperfusion injury under a mild decrease in core liver temperature of 10 degrees C by in situ hypothermic perfusion during ischemia.
Liver ischemia was induced in pigs by total hepatic vascular exclusion with concomitant in situ perfusion with hypothermic (4 degrees C) Ringer-glucose (cold perfused group, core liver temperature maintained at 28 degrees C), with normothermic (38 degrees C) Ringer-glucose (warm perfused group) or without in situ perfusion (control group).
In the cold perfused, warm perfused, and control groups, 24-hour survival was 5/5, 0/5, and 3/5, respectively. Hemodynamic parameters in the cold perfused group remained stable, whereas pigs in both other groups required circulatory support. Plasma AST and interleukin-6 levels were lower in the cold perfused group than in both other groups. Hepatocellular function was best preserved in the cold perfused group as indicated by complete recovery of bile production during reperfusion and no loss of indocyanine green clearance capacity. In both other groups, bile production and indocyanine green clearance capacity were reduced significantly. The hyaluronic acid uptake capacity of pigs in the cold perfused group or control group did not differ, indicating preserved sinusoidal endothelial cell function. Histopathologic injury scores during reperfusion were significantly lower in the cold perfused group when compared to both other groups.
A mild decrease in core liver temperature of 10 degrees C by in situ hypothermic liver perfusion during ischemia protects the liver from ischemia/reperfusion injury. This protection appears to be related to cooling of the liver rather than to the washout of blood during perfusion.
我们试图通过在缺血期间进行原位低温灌注,使肝脏核心温度轻度降低10℃,来评估肝脏缺血/再灌注损伤。
通过完全肝血管阻断诱导猪肝脏缺血,同时分别进行低温(4℃)林格氏葡萄糖原位灌注(冷灌注组,肝脏核心温度维持在28℃)、常温(38℃)林格氏葡萄糖原位灌注(温灌注组)或不进行原位灌注(对照组)。
冷灌注组、温灌注组和对照组的24小时生存率分别为5/5、0/5和3/5。冷灌注组的血流动力学参数保持稳定,而其他两组的猪都需要循环支持。冷灌注组的血浆谷草转氨酶和白细胞介素-6水平低于其他两组。冷灌注组的肝细胞功能保存最佳,表现为再灌注期间胆汁分泌完全恢复,吲哚菁绿清除能力无损失。其他两组的胆汁分泌和吲哚菁绿清除能力均显著降低。冷灌注组或对照组猪的透明质酸摄取能力无差异,表明肝窦内皮细胞功能保存。与其他两组相比,冷灌注组再灌注期间的组织病理学损伤评分显著更低。
缺血期间通过原位低温肝脏灌注使肝脏核心温度轻度降低10℃可保护肝脏免受缺血/再灌注损伤。这种保护作用似乎与肝脏降温有关,而非与灌注期间的血液冲洗有关。