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

Abstract

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.

Induction of Robust Future Liver Remnant Hypertrophy Before Hepatectomy With a Modified Liver Venous Deprivation Technique Using a Trans-venous Access for Hepatic Vein Embolization

“…Portal vein pressures were measured before PVE and after liver venous deprivation (end of the procedure). Right portal vein embolization was performed before hepatic vein embolization, because hepatic vein embolization reduces portal flow in the embolized segment making portal vein embolization more at risk for non-target embolization as demonstrated in two animal studies ( 15 , 16 ). Although both a left or right portal vein approach can be used for right PVE, we prefer using a contralateral approach, which makes the procedure technically easier (e.g., avoiding catheter kinking), and is safer in case of right liver biliary tree dilatation as observed in Klatskin tumors ( 17 ).…”

Study of Morphological Changes in Rat Liver Caused by Occlusion of Inferior Vena Cava

“…After opening the abdominal cavity, the presence of varicose veins of the anterior abdominal wall, ascetic fluid in the abdominal cavity, and the presence of changes in the size of the liver and spleen were visually assessed. Indicators of abdominal circumference, the development of abdominal varicose veins, pathological changes in the liver and spleen, changes in liver function, and hypertension in the inferior vena cava were regarded as signs of a simulated Budd-Chiari syndrome, 6 as a control for this assessment, previously described information was also taken into account. 17…”

“…4,5 The development of Budd-Chiari syndrome model was mainly achieved via surgical reduction of the diameter of the inferior vena cava or the occlusion of the hepatic branches by the endovascular method. [4][5][6] There are two options for imitating the Budd-Chiari syndrome: hepatic vein thrombosis (the so-called classic Budd-Chiari syndrome) and hepatic vena cava-Budd-Chiari syndrome. 7 The effect of hypertension on hepatic vessels has been well described for classical models, 8 including models based on the endovascular approach.…”

“…7 The effect of hypertension on hepatic vessels has been well described for classical models, 8 including models based on the endovascular approach. 6 There is a range of reports on the link between the development of persistent morphological changes in the vessels and the liver with the degree of narrowing of the caudal inferior vena cava as well as the duration of violations of blood outflow. 5,9 However, there are no data on the effect of increased sinusoidal pressure on the portal tract, morphological changes over time, and survival rate depending on the degree of vasoconstriction.…”

Experimental model of portal hypertension and esophagogastric varices in minipigs: pressure and endoscopic pilot study

“…There are several methods capable to reproduce one of the three types of portal hypertension (i.e., prehepatic and posthepatic), each with its own characteristics, results and applications 11 . Biliary tract ligation, hepatic artery embolization with 80% alcohol, infusion of non-radioactive colored tracer microspheres, intoxication by carbon tetrachloride (CCL4) and thioacetamide (TAA) are the most used intrahepatic portal hypertension models, while the gradual occlusion of the inferior vena cava (gOIVC) is the standard model for posthepatic portal hypertension [12][13][14][15][16][17][18][19] .…”