Clinical and experimental study of regeneration of nonembolized lobe after portal vein embolization

本研究证实了门静脉栓塞后未栓塞肝叶再生的可能机制。临床研究：门静脉右支栓塞后，门静脉左支血流量明显增加，管径也增大。超声测量显示，右门静脉栓塞导致第2段、第3段和第4段门静脉分支直径增加约150%。血清IL-6浓度在门静脉栓塞后3 h内显著升高，24 h达高峰，随后逐渐下降。肿瘤坏死因子（TNF）-α和肝细胞生长因子（HGF）浓度保持不变。实验研究：人肝窦微血管内皮细胞（HLSEC）和人脐静脉内皮细胞（HUVEC）在硅室上培养，硅室在整个膜上150%拉伸。持续机械牵张后，内皮细胞培养上清中IL-6浓度显著升高，而TNF-α和HGF浓度无明显变化。NF κ B活化后IL-6 mRNA表达增加。结论：这些发现表明门静脉栓塞扩张了未栓塞叶的门静脉分支，使肝血管暴露于拉伸应力。这种血流动力学变化可能是内皮细胞释放白细胞介素-6的触发因素，并有助于激活未栓塞肺叶的再生级联反应。

This study demonstrated possible mechanism of liver regeneration in the nonembolized lobe after portal vein embolization. Clinical study : After right portal vein embolization, the blood flow of the left portal vein significantly increased, and the diameter of this vein also enlarged. Ultrasonographic measurement revealed that right portal vein embolization induces approximately 150% increase in diameter of the segment 2, segment 3, and segment 4 portal branches. Serum interleukin-6 concentrations significantly increased within 3 hours after portal vein embolization, peaked at 24 hours, then gradually decreased. The concentrations of tumor necrosis factor (TNF)-α and hepatocyte growth factor (HGF) remained unchanged. Experimental study : Human liver sinusoidal microvascular endothelial cells (HLSECs) and human umbilical vein endothelial cells (HUVECs) were cultured on the silicon chamber which were 150% stretched over the entire membrane. After this continuous mechanical stretch, the concentration of interleukin-6 in the supernatant of endothelial cells significantly increased, while the concentrations of TNF-α and HGF were unchanged. Interleukin-6 mRNA expression followed activation of NF κ B. Conclusion : These findings indicate that portal vein embolization dilates the portal branches in the nonembolized lobe, exposing hepatic vasculature to stretch stress. This hemodynamic change may act as a trigger for interleukin-6 release from endothelial cells and contribute to the activation of regenerative cascade in the nonembolized lobes.