Dirsch Olaf, Madrahimov Nodir, Chaudri Naved, Deng Meihong, Madrahimova Fotima, Schenk Andrea, Dahmen Uta
Institute of Pathology, University of Cologne [corrected] Germany.
Transplantation. 2008 Mar 15;85(5):748-56. doi: 10.1097/TP.0b013e31816631f9.
Live liver donation requires extended liver resection in the donor with transection of the middle hepatic vein. This leads to focal outflow obstruction in the remnant liver or the partial graft. This study was designed to characterize the pathophysiological correlate of focal outflow obstruction in a small-for-size liver and its course of recovery in a rat model.
Ligation of the right median hepatic vein was combined with 50% hepatectomy. Microcirculation was visualized by orthogonal polarization spectroscopy after each operative step and before killing on days 1, 2, and 7. Histologic evaluation included morphological assessment, immunohistochemical determination of proliferation using BrdU, and laminin and von Willebrand factor expression, which both indicate vascularization of sinusoids.
After ligation of the right median hepatic vein, congestion was visible and no sinusoidal blood flow was detected in the obstruction zone. By day 1 confluent centrilobular necrosis developed. Sinusoidal perfusion in the obstruction zone recovered partially. Many dilated vascularized sinusoidal canals connecting the obstruction zone with the normal zone were visible. Proliferative activity in the obstruction zone was markedly reduced compared with the normal zone. By day 7, liver parenchyma in the obstruction zone looked normal as did sinusoidal perfusion. In the border zone, few dilated vascular canals were apparent.
Confluent centrilobular necrosis in the early postoperative phase, resulting from focal outflow obstruction, may be crucial for the development of a small-for-size syndrome. The exclusion of the outflow-obstructed zone from the functional liver mass during preoperative radiological risk assessment seems to be the logical consequence. Recovery of focal outflow obstruction occurs spontaneously by means of dilated sinusoids in the border zone, forming vascularized sinusoidal canals, which could serve as intrahepatic anastomosis.
活体肝移植供体需要进行扩大肝切除术并横断肝中静脉。这会导致残余肝脏或部分移植物出现局灶性流出道梗阻。本研究旨在在大鼠模型中描述小体积肝脏局灶性流出道梗阻的病理生理相关性及其恢复过程。
将右肝中静脉结扎与50%肝切除术相结合。在每个手术步骤后以及术后第1天、第2天和第7天处死前，通过正交偏振光谱法观察微循环。组织学评估包括形态学评估、使用BrdU进行增殖的免疫组化测定以及层粘连蛋白和血管性血友病因子表达，这两者均表明肝血窦的血管化。
右肝中静脉结扎后，可见充血，梗阻区域未检测到肝血窦血流。术后第1天出现融合性小叶中心坏死。梗阻区域的肝血窦灌注部分恢复。可见许多扩张的、血管化的肝血窦通道将梗阻区域与正常区域相连。与正常区域相比，梗阻区域的增殖活性明显降低。到第7天，梗阻区域的肝实质看起来正常，肝血窦灌注也正常。在边界区域，可见少数扩张的血管通道。
术后早期由局灶性流出道梗阻导致的融合性小叶中心坏死可能对小体积综合征的发生至关重要。术前放射学风险评估中从功能性肝体积中排除流出道梗阻区域似乎是合理的结果。局灶性流出道梗阻通过边界区域扩张的肝血窦自发恢复，形成血管化的肝血窦通道，可作为肝内吻合。
