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首页> 外文期刊>Transplantation: Official Journal of the Transplantation Society >Recovery of liver perfusion after focal outflow obstruction and liver resection.
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Recovery of liver perfusion after focal outflow obstruction and liver resection.

机译:局灶性流出道梗阻和肝切除术后肝灌注恢复。

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BACKGROUND.: 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. METHODS.: 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. RESULTS.: 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. CONCLUSION.: 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.
机译:背景:活体肝捐赠需要在供体中扩大肝切除术并切除肝中静脉。这导致残余肝或部分移植物中的局灶性流出阻塞。这项研究旨在表征小型肝脏中局灶性流出道梗阻的病理生理相关性及其在大鼠模型中的恢复过程。方法:右肝中静脉结扎术结合50%肝切除术。在每个手术步骤之后以及在第1、2和7天杀死之前,通过正交极化光谱法观察微循环。组织学评估包括形态学评估,使用BrdU进行的免疫组织化学测定增殖以及层粘连蛋白和von Willebrand因子表达,这都表明了正弦曲线的血管化。结果:结扎右肝中静脉后,可见阻塞,在梗阻区未检测到正弦血流。到第1天,融合小叶坏死发展。阻塞区的正弦灌注部分恢复。可以看到许多连接梗阻区和正常区的扩张的血管化窦道。与正常区域相比,阻塞区域的增殖活性明显降低。到第7天,梗阻区的肝实质看起来很正常,正弦曲线灌注也一样。在边界区,几乎没有扩张的血管。结论:局灶性流出道梗阻引起的术后早期融合小叶坏死可能对小型综合征的发展至关重要。在术前放射风险评估期间,从功能性肝肿块中排除流出阻塞区似乎是合理的结果。局灶性流出道梗阻的恢复通过边界区域的扩张正弦波自发发生,形成血管化正弦波管,可作为肝内吻合术。

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