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 in | Molecular medicine reports Vol. 9; no. 2; pp. 607 - 613 |
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Main Authors | , , , , , , , , , |
Format | Journal Article |
Language | English |
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D.A. Spandidos
01.02.2014
Spandidos Publications Spandidos Publications UK Ltd |
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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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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 |
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