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

肝部分切除术（PHx）后损伤再生的概念和未直接损伤的肝细胞再生的原因尚不清楚。血流产生的切应力在血管重塑机制中起重要作用，门静脉压力反映了切应力。本研究旨在确定急性门静脉高压症（APH）是否可以成为肝再生的触发因素，在大鼠模型PHx后的切应力。门静脉压力在70%和90%PHx后立即升高，在术后第3天（POD）达到峰值，此后随着肝再生的减少而成比例下降。即使在POD7，90%PHx后的门静脉压力也显著高于不含70%PHx后的门静脉压力。肝窦内皮细胞（SEC）上I类抗原的梯度表达仅见于健康大鼠肝门静脉压力最高的门静脉周围区。而肝切除术后，从门静脉周围区到中央静脉区均有表达。这些结果表明，APH作为PHx后的切应力不仅可能成为肝细胞再生的触发器，而且也是SEC再生的触发器，并且过量的APH导致肝功能障碍。

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.