Development of a canine model with diffuse hepatic vein obstruction (Budd‑Chiari syndrome) via endovascular occlusion

Shen,Bin; Zhang,Qingqiao; Wang,Xiaolong; Xu,Hao; Zu,Maoheng; Wu,Meng; Gao,Zhikang; Wang,Wenliang; Xiao,Jinchang; Wang,Yong

doi:10.3892/mmr.2013.1868

Development of a canine model with diffuse hepatic vein obstruction (Budd‑Chiari syndrome) via endovascular occlusion

Authors:
- Bin Shen
- Qingqiao Zhang
- Xiaolong Wang
- Hao Xu
- Maoheng Zu
- Meng Wu
- Zhikang Gao
- Wenliang Wang
- Jinchang Xiao
- Yong Wang
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Affiliations: Department of Interventional Radiology, The Affiliated Hospital of Xuzhou Medical College, Xuzhou, Jiangsu 221006, P.R. China
Published online on: December 17, 2013 https://doi.org/10.3892/mmr.2013.1868
Pages: 607-613

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Abstract

The aim of the present study was to develop a reliable and reproducible canine model to mimic human diffuse hepatic vein obstruction (Budd‑Chiari syndrome, BCS). A total of 24 canines were divided into an experimental (n=18) and a control (n=6) group. Under the guidance of digital subtraction angiography, a balloon catheter was delivered to the target hepatic vein (the common trunk of the left hepatic and middle hepatic veins) via the right external jugular vein. The balloon was inflated to completely block the vessels. For the canines in the experimental group, a mixture of N‑butyl‑cyanoacrylate (NBCA) and lipiodol (3‑5 ml) was injected via the balloon catheter. Canines in the control group were injected with equal volumes of normal saline. Liver function and pathology were examined at 4, 6 and 8 weeks following surgery. BCS was successfully established in all members of the experimental group and there were no serious complications in either group. The left and middle hepatic veins and common trunk were completely obstructed at 4, 6 and 8 weeks following surgery in the experimental group, while in the control group, the hepatic vein remained unobstructed at 4 weeks. There was hepatocyte congestion and edema at 4 weeks following surgery in the experimental group and the edema became aggravated following 6 weeks. At 8 weeks following surgery, there was necrosis of hepatocytes and significant thickening of the hepatic vein tunica intima in addition to an increased number of elastic fibers. In conclusion, the present study demonstrates that a reliable and reproducible canine model of BCS can be developed by endovascular obstruction of the hepatic vein.

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