Rozga J, Jeppsson B, Bengmark S
Eur Surg Res. 1986;18(5):302-11. doi: 10.1159/000128539.
Portal branch ligation (PBL) is known to induce a rapid and progressive atrophy in the liver parenchyma without portal blood flow and compensatory hyperplasia in the segments receiving the whole portal flow. In this study, the hepatotrophic effect of portal blood was studied in rats with PBL and after this procedure was combined with different portosystemic shunts. After 2 weeks, the most severe atrophy was found in ligated lobes of rats with PBL alone. In shunted animals, the atrophy was significantly inhibited and in relation to the magnitude of portal flow bypassed the liver. This suggests that in shunted rats, the portal-bone hepatotrophic factors undergo systemic recirculation and affect the liver by way of the hepatic artery. Simultaneously, in PBL + shunt rats, the rate of atrophy normally induced by a shunt was also dependent on the amount of portal blood available to this part of the liver. By a balance between these 2 processes, the total liver mass was maintained at the level found in sham PBL + shunt control rats.
门静脉分支结扎术（PBL）已知会在无门静脉血流的肝实质中引发快速且进行性的萎缩，并在接受全部门静脉血流的肝段中引发代偿性增生。在本研究中，对行PBL的大鼠以及该手术与不同门体分流术联合后的大鼠，研究了门静脉血的肝营养作用。2周后，仅行PBL的大鼠结扎叶出现最严重的萎缩。在分流动物中，萎缩受到显著抑制，且与绕过肝脏的门静脉血流程度相关。这表明在分流大鼠中，门静脉源性肝营养因子会进行体循环，并通过肝动脉影响肝脏。同时，在PBL + 分流大鼠中，分流正常诱导的萎缩速率也取决于该部分肝脏可获得的门静脉血量。通过这两个过程之间的平衡，肝脏总质量维持在假手术PBL + 分流对照大鼠的水平。
