Rozga J, Jeppsson B, Bengmark S
Am J Pathol. 1986 Nov;125(2):300-8.
The effects of portal occlusion on the liver have been differently reported in different studies. The authors therefore reevaluated a model of portal branch ligation (PBL) in the rat. Histologic appearance, DNA synthetic activity, labeling count, and mitotic index were serially evaluated in both ligated and nonligated parts of the liver after interruption of the portal flow to one fourth, one third, and two thirds of the liver mass. The authors confirmed the presence of compensatory hyperplasia induced in the nonligated liver lobe(s) by PBL, and its intensity was roughly proportional to the amount of liver tissue devoid of portal perfusion. Portal-deprived liver tissue underwent a rapid and progressive atrophy, and, by the end of the first week, the weight of this part had decreased 10-fold. By a balance between atrophy and compensatory growth, the total liver weight was maintained at the level of sham-operated animals throughout the experiment. PBL invariably resulted in early centrilobular necrosis, which occupied 15-24% of the ligated lobe(s). However, already after 4 days it was almost totally resorbed and did not appear de novo. PBL was not followed by local collateralization.
门静脉闭塞对肝脏的影响在不同研究中有不同报道。因此，作者重新评估了大鼠门静脉分支结扎（PBL）模型。在门静脉血流中断至肝脏质量的四分之一、三分之一和三分之二后，对肝脏结扎和未结扎部分的组织学外观、DNA合成活性、标记计数和有丝分裂指数进行了连续评估。作者证实了PBL在未结扎肝叶中诱导了代偿性增生，其强度大致与缺乏门静脉灌注的肝组织量成正比。门静脉缺失的肝组织经历了快速且渐进性的萎缩，到第一周结束时，该部分的重量下降了10倍。通过萎缩与代偿性生长之间的平衡，整个实验过程中肝脏总重量维持在假手术动物的水平。PBL总是导致早期小叶中央坏死，其占结扎肝叶的15%-24%。然而，4天后几乎完全吸收，且未再次出现。PBL后未出现局部侧支循环形成。
