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

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 angiog...

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Published inMolecular medicine reports Vol. 9; no. 2; pp. 607 - 613
Main Authors SHEN, BIN, ZHANG, QINGQIAO, WANG, XIAOLONG, XU, HAO, ZU, MAOHENG, WU, MENG, GAO, ZHIKANG, WANG, WENLIANG, XIAO, JINCHANG, WANG, YONG
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LanguageEnglish
Published Greece D.A. Spandidos 01.02.2014
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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.
AbstractList 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.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.
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 A-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.
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.
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 A-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. Key words: animal model, Budd-Chiari syndrome, hepatic vein, portal hypertension, hepatic function
Audience Academic
Author ZHANG, QINGQIAO
ZU, MAOHENG
XIAO, JINCHANG
WANG, XIAOLONG
WU, MENG
WANG, WENLIANG
WANG, YONG
SHEN, BIN
XU, HAO
GAO, ZHIKANG
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CitedBy_id crossref_primary_10_1016_j_bbadis_2018_07_018
crossref_primary_10_1590_acb370103
crossref_primary_10_3389_fradi_2021_736056
crossref_primary_10_1016_j_jceh_2022_06_001
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Snippet 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,...
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,...
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SubjectTerms Angiography
animal model
Animals
Balloon catheters
Budd-Chiari syndrome
Budd-Chiari Syndrome - diagnostic imaging
Budd-Chiari Syndrome - genetics
Budd-Chiari Syndrome - pathology
Cardiovascular system
Care and treatment
Catheters
Diagnosis
Disease Models, Animal
Dogs
Edema
Health aspects
hepatic function
Hepatic vein
Hepatic vein thrombosis
Hepatic Veins - diagnostic imaging
Hepatic Veins - pathology
Hepatocytes
Humans
Jugular vein
Laboratory animals
Liver
Occlusion
portal hypertension
Radiography
Risk factors
Rodents
Studies
Surgery
Ultrasonic imaging
Veins & arteries
Velocity
Title Development of a canine model with diffuse hepatic vein obstruction (Budd-Chiari syndrome) via endovascular occlusion
URI https://www.ncbi.nlm.nih.gov/pubmed/24345960
https://www.proquest.com/docview/1932462256
https://www.proquest.com/docview/1490750952
Volume 9
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