Sokirchenko I A
Biull Eksp Biol Med. 1993 Nov;116(11):548-50.
Portal vein occlusion leads to accumulation of intestinal endotoxin in the portal vein that may be a trigger for release of liver macrophage products from the cells and then for damage to hepaparenchyma. There is activation of Kupffer cells (KC) after ischemia, increasing the volume of second lysosomes, severe erythrophagia was also seen. Moreover, there is an increase in KC count and appearance of young liver macrophages. The rise of KC population counts due to the increased number of functional element play a positive role in clearance of intestinal endotoxin and liver defence for ischemic and recirculatory organ damage.
门静脉阻塞会导致门静脉中肠内毒素的蓄积，这可能是触发肝巨噬细胞产物从细胞中释放，进而损伤肝实质的一个因素。缺血后库普弗细胞（KC）被激活，继发性溶酶体体积增大，还可见严重的红细胞吞噬现象。此外，KC数量增加，出现年轻的肝巨噬细胞。由于功能元件数量增加导致的KC群体计数升高，在清除肠内毒素以及肝脏对缺血和再循环器官损伤的防御中发挥着积极作用。
