Department of Radiology, Academic Medical Center, University of Amsterdam, Amsterdam, the Netherlands.
Hepatobiliary Pancreat Dis Int. 2013 Dec;12(6):622-9. doi: 10.1016/s1499-3872(13)60098-3.
Portal vein embolization not only induces hypertrophy of the non-embolized liver, but also enhances tumor growth. The latter could be prevented by embolizing the hepatic arteries supplying the tumor-bearing liver segments. This study aimed to determine the effects of transcatheter arterial embolization (TAE) on tumor volume and liver regeneration in a rabbit VX2 tumor model.
Twenty-three rabbits underwent subcapsular tumor implantation with a VX2 tumor. Two weeks after implantation, 18 rabbits were used for TAE experiments, 5 were for sham controls. Tumor response and liver regeneration response of the embolized cranial and non-embolized caudal liver lobes were assessed by CT volumetry, liver to body weight index, and the amount of proliferating hepatocytes.
All super-selective arterial tumor embolization procedures were performed successfully. Despite embolization, the tumor volume increased after an initial steady state. The tumor volume after embolization was smaller than that of the sham group, but this difference was not significant. Massive necrosis of the tumor, however, was seen after embolization, without damage of the surrounding liver parenchyma. There was a significant atrophy response of the tumor bearing cranial lobe after super-selective arterial embolization of the tumor with a concomitant hypertrophy response of the non-embolized, caudal lobe. This regeneration response was confirmed histologically by a significantly higher number of proliferating hepatocytes on the Ki-67 stained slides.
Super-selective, bland arterial coil embolization causes massive necrosis of the tumor, despite increase of volume on CT scan. Atrophy of the tumor bearing liver lobe is seen after arterial embolization of the tumor with a concomitant hypertrophy response of the non-embolized lobe, despite absence of histological damage of the tumor-surrounding liver parenchyma.
门静脉栓塞不仅会导致未栓塞肝脏的肥大，还会增强肿瘤的生长。后者可以通过栓塞供应肿瘤所在肝段的肝动脉来预防。本研究旨在确定经导管动脉栓塞 (TAE) 对兔 VX2 肿瘤模型中肿瘤体积和肝再生的影响。
23 只兔子进行了 VX2 肿瘤的包膜下肿瘤植入。植入后 2 周，18 只兔子用于 TAE 实验，5 只用于假手术对照。通过 CT 体积测量、肝体比和增殖肝细胞的数量评估栓塞的颅侧和未栓塞的尾侧肝叶的肿瘤反应和肝再生反应。
所有超选择性动脉肿瘤栓塞术均成功完成。尽管进行了栓塞，但肿瘤体积在初始稳定后仍会增加。栓塞后的肿瘤体积小于假手术组，但差异无统计学意义。然而，栓塞后可见肿瘤大量坏死，而周围肝实质未受损。超选择性动脉栓塞肿瘤后，肿瘤负荷的颅侧肝叶出现明显萎缩反应，同时非栓塞的尾侧肝叶出现肥大反应。Ki-67 染色切片上增殖肝细胞数量明显增加，组织学上证实了这种再生反应。
尽管 CT 扫描上肿瘤体积增加，但超选择性、温和的动脉线圈栓塞会导致肿瘤大量坏死。肿瘤动脉栓塞后，肿瘤负荷的肝叶会出现萎缩，尽管肿瘤周围肝实质没有组织学损伤，但非栓塞的肝叶会出现肥大反应。
