Acute portal hypertention as a Trigger of liver regeneration following partial hepatectomy

肝部分切除术（PHx）后损伤再生的概念以及未直接损伤的肝细胞再生的原因尚不清楚，已知血流产生的剪切应力在血管重塑机制中起重要作用，门静脉压力反映剪切应力。本研究旨在确定急性门脉高压（APH）是否可以在大鼠PHx模型中作为剪切应力成为肝脏再生的触发因素。在70%和90% PHx后，门静脉压力立即升高，在术后一天（POD）3达到峰值，此后随着肝再生的减少成比例下降。即使在POD7上，90% PHx后的门静脉压力也明显高于未70% PHx的门静脉压力。I类抗原在正常大鼠肝脏门静脉压力最大的门静脉周围区呈梯度表达。然而，肝切除术后，这些表达从门静脉周围区域到中心静脉区域检测到。以上结果提示，APH作为PHx后的剪切应力不仅可能成为肝细胞再生的触发因素，还可能成为SEC再生的触发因素，APH过剩可引起肝功能障碍。

The concept of injury regeneration after partial hepatectomy(PHx), and the reason hepatocytes that have not been directly injured regenerate, remain unclear, It is known that shear stress resulting from blood flow plays an important role in the mechnism of remodeling blood vessels, and portal pressure reflects shear stress. This study was conducted to determine whether acute portal hypertention(APH) can become a trigger of liver regeneration as shear stress following PHx in a rat model. Portal pressures became elevated immediately after 70% and 90% PHx, peaking on postoperative day (POD)3, and thereafter decreasing in proportion to the diminution of liver regeneration. The portal pressures after 90% PHx were significantly higher than those after without 70% PHx even on POD7. The gradient expressions of class I antigen on sinusoidal endothelial cells(SEC) were found only in the periportal area, which has the highest portal pressure in the healthy rat liver. However, after hepatectomy these expressions were detected from the periportal area tothe central venous area. These results suggest that APH as shear stress following PHx may not only become a trigger of hepatocyte regeneration, but also of SEC regeneration, and that surplus APH induces liver dysfunction.