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

Background/Aims: Prehepatic portal hypertension caused by extrahepatic port al vein occlusion is a situation in which hepatocytes are not damaged by di sease despite the fact that portal blood is unable to reach them due to por tal vein occlusion. We explored the patency of intrahepatic portal vein bra nches after extrahepatic portal vein occlusion for the possibility of revas cularization by splenoportal shunt. Methodology: Prehepatic portal hypertension was induced in 8 mini-pigs by e xternal compression of the portal vein with a device consisting of an infla table silicone balloon mounted on a silicone cuff and attached to a subcuta neous chamber. Another device consisting of cannula and a subcutaneous cham ber was placed into the splenic vein for portal pressure monitoring and por tal venograms. Both devices were placed during laparotomy with their chambe rs positioned subcutaneously. Portal vein compression was initiated one wee k later and was accomplished in two steps. Extrahepatic portal vein occlusi on and the patency of intrahepatic portal vein branches were confirmed by d irect portal venography. Alteration of the intrahepatic portal bed was exam ined at necropsy after 4 weeks, checking for the presence of occlusion or t hrombosis. Results: Portal vein occlusion was achieved in 5 animals, while severe sten osis was demonstrated in the remaining three. Portal venograms demonstrated patency of the lobar portal vein branches filled by hepatopetal collateral s around the occluded port al vein. All intrahepatic branches were free of thrombus at gross examination. Conclusions: In the absence of the hepatic parenchymal disease, lobar intra hepatic portal vein branches remain patent despite truncal portal vein occl usion and are supplied by rapidly developed hepatopetal collaterals.