Keller G A, West M A, Cerra F B, Simmons R L
Ann Surg. 1985 Jan;201(1):87-95.
The etiology of hepatic insufficiency associated with the multiple systems organ failure (MSOF) syndrome is unclear. The authors have investigated the possibility that a macrophage/Kupffer cell mediated modulation of hepatocyte function may play a role in this phenomenon. Isolated rat hepatocytes were cultured, and their rate of protein synthesis was measured by cpm of 3H leucine incorporation into protein. Nonparenchymal rat liver cells (NPC) comprised of 35-40% Kupffer cells were added to hepatocytes to establish a co-culture with or without endotoxin. Neither NPC alone nor endotoxin alone affected hepatocyte protein synthesis. However, in the presence of endotoxin, NPC caused a marked diminution of hepatocyte protein synthesis (4,396 +/- 449 cpm) compared with control hepatocytes (10,943 +/- 623 cpm). No change in microscopic morphology or ability to exclude trypan blue occurred. This modulation of hepatocyte function by an endotoxin stimulated Kupffer cell preparation may, in part, represent the mechanism of hepatic insufficiency associated with the MSOF syndrome.
与多系统器官衰竭（MSOF）综合征相关的肝功能不全的病因尚不清楚。作者研究了巨噬细胞/库普弗细胞介导的肝细胞功能调节可能在这一现象中起作用的可能性。培养分离的大鼠肝细胞，通过3H亮氨酸掺入蛋白质的每分钟计数（cpm）来测量其蛋白质合成速率。将由35% - 40%库普弗细胞组成的大鼠非实质肝细胞（NPC）添加到肝细胞中，以建立有无内毒素的共培养体系。单独的NPC或单独的内毒素均不影响肝细胞蛋白质合成。然而，在内毒素存在的情况下，与对照肝细胞（10,943 +/- 623 cpm）相比，NPC导致肝细胞蛋白质合成显著减少（4,396 +/- 449 cpm）。微观形态或排除台盼蓝的能力没有变化。内毒素刺激的库普弗细胞制剂对肝细胞功能的这种调节可能部分代表了与MSOF综合征相关的肝功能不全的机制。
