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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

安全广泛肝切除门静脉分支栓塞的基础与临床研究

基本信息

批准号：
09671298
负责人：
NAGINO Masato
金额：
$ 1.92万
依托单位：
Nagoya University
依托单位国家：
日本
项目类别：
Grant-in-Aid for Scientific Research (C)
财政年份：
1997
资助国家：
日本
起止时间：
1997 至 1998
项目状态：
已结题

来源：
https://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-09671298/
关键词：
Percutaneous transhepatic protal vein embolization Trisegment portal vein embolization Ipsilateral approach Portal plus arterial embolization Portal blood flow velocity Doppler ultrasound Liver regeneration Apoptosis 肝門部胆肝癌胆嚢癌肝切除術

项目摘要

[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.

[临床研究] 1）我们开发了三段门静脉栓塞术，为右或左肝三段切除术做准备。右三节段栓塞，栓塞左内侧、右前、右后段；左三节段栓塞术涉及左侧外节、左侧内侧节和右侧前节。三段栓塞使肝三段切除术变得安全。 2）设计了门静脉加动脉栓塞（双重栓塞），以扩大功能储备较差患者的广泛肝切除适应症。这种新的干预措施可以在非栓塞肝段中产生相当大的肥大。 3)使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，栓塞后非栓塞肝段的肥大率可以根据门静脉血流速度增加的程度来预测。 4) 通过Angio-CT，我们发现门静脉栓塞后，栓塞肝段的肝动脉血流量立即增加。[实验研究] 1) 我们利用门支结扎大鼠模型，研究了门静脉栓塞后非栓塞肝段肥大的机制。从聚合酶活性和线粒体功能的角度来看，门静脉栓塞以类似于部分肝切除术的方式诱导非栓塞肝段中的肝细胞增殖。 2）我们还利用门静脉分支结扎大鼠模型研究了门静脉栓塞后栓塞肝段萎缩的机制。这种萎缩是肝细胞凋亡的结果，而不是坏死。此外，我们还阐明了核鞘磷脂的分解以及细胞核中神经酰胺和/或鞘氨醇的积累可能会诱导体内肝细胞的凋亡。