Intrahepatic portal vein branches after extrahepatic portal vein occlusion. Experimental study

Background/Aims: Prehepatic portal hypertension caused by extrahepatic portal vein occlusion is a situation in which hepatocytes are not damaged by disease despite the fact that portal blood is unable to reach them due to portal vein occlusion. We explored the patency of intrahepatic portal vein branches after extrahepatic portal vein occlusion for the possibility of revascularization by splenoportal shunt. Methodology: Prehepatic portal hypertension was induced in 8 mini-pigs by external compression of the portal vein with a device consisting of an inflatable silicone balloon mounted on a silicone cuff and attached to a subcutaneous chamber. Another device consisting of cannula and a subcutaneous chamber was placed into the splenic vein for portal pressure monitoring and portal venograms. Both devices were placed during laparotomy with their chambers positioned subcutaneously. Portal vein compression was initiated one week later and was accomplished in two steps. Extrahepatic portal vein occlusion and the patency of intrahepatic portal vein branches were confirmed by direct portal venography. Alteration of the intrahepatic portal bed was examined at necropsy after 4 weeks, checking for the presence of occlusion or thrombosis. Results: Portal vein occlusion was achieved in 5 animals, while severe stenosis was demonstrated in the remaining three. Portal venograms demonstrated patency of the lobar portal vein branches filled by hepatopetal collaterals around the occluded portal vein. All intrahepatic branches were free of thrombus at gross examination. Conclusions: In the absence of the hepatic parenchymal disease, lobar intrahepatic portal vein branches remain patent despite truncal portal vein occlusion and are supplied by rapidly developed hepatopetal collaterals.