安全な広範肝切除を目的とした門脈枝塞栓術の基礎的および臨床的研究

【临床研究】1)我们开发了门静脉三节段栓塞术，为左、右肝三节段切除术做准备。在右三节段栓塞中，左内段、右前段和右后段被栓塞；在左三节段栓塞，左外侧，左内侧，和右前段受累。三节段栓塞使肝三节切除术安全。2)设计门脉加动脉栓塞（双栓塞），以扩大功能储备差患者广泛肝切除的适应证。这种新的干预可以在未栓塞的肝段产生相当大的肥厚。3)应用多普勒超声估计栓塞后门静脉血流速度。这项研究清楚地表明，栓塞后未栓塞肝段的肥厚率可以从门静脉血流速度的增加程度来预测。4)通过血管ct，我们发现门静脉栓塞后栓塞肝段的肝动脉血流立即增加。【实验研究】1)采用门脉支结扎大鼠模型，研究门静脉栓塞后未栓塞肝段肥厚的发生机制。从聚合酶活性和线粒体功能的角度来看，门静脉栓塞诱导未栓塞肝段肝细胞增殖的方式与肝部分切除术相似。2)我们还采用门脉支结扎大鼠模型，研究了门脉栓塞后肝段萎缩的机制。这种萎缩是由肝细胞凋亡引起的，而不是坏死。此外，我们已经阐明，核鞘磷脂分解与神经酰胺和/或鞘磷脂在核内的积累可能诱导体内肝细胞凋亡。

[Clinical Study] 1) We have developed trisegment portal vein embolization in preparation for right or left hepatic trisegmentectomy. In right trisegment embolization, the left medial, right anterior, and right posterior segments were embolized ; in left trisegment embolization, the left lateral, left medial, and right anterior segments were involved. Trisegment enibolization has made hepatic trisegmentectomy safe. 2) Portal plus arterial embolization (dual embolization) was devised, in order to expand the indication of extensive liver resection for patients with poor functional reserve. This new intervention can produce sizable hypertrophy in the non-embolized hepatic segments. 3) Portal blood flow velocity after embolization was estimated using Doppler ultrasound. This study clearly has demonstrated that the hypertrophy rate of non-embolized hepatic segments after embolization is predictable from the extent of the increase in portal blood flow velocity. 4) With Angio-CT, we have found an immediate increase in the hepatic artery blood flow in the embolized hepatic segments after portal vein embolization.[Experimental Study] 1) We have investigated the mechanism of hypertrophy in the non-embolized hepatic segments after portal vein embolization, using portal branch ligated rat model.. From the view point of polymerase activity and mitochondrial function, portal vein embolization induces hepatocyte proliferation in the non-embolized hepatic segments in a way similar to partial hepatectomy. 2) We have also studied the mechanism of atrophy in the embolized hepatic segments after portal vein embolization, using portal branch ligated rat model.. This atrophy results from, not necrosis, apoptosis of hepatocyte. In addition, we have elucidated that nuclear sphingomyelin breakdown with an accumulation of ceramide and/or sphingosine in nuclei may induce the apoptosis of hepatocyte in vivo.