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Angiographic, hemodynamic, and histologic evaluation of portal hypertension and periportal fibrosis induced in the dog by intraportal polyvinyl alcohol injections.

Intrahepatic periportal fibrosis and portal hypertension were produced in the dog by repeated intraportal injection of a polyvinyl alcohol suspension over a two- to six-month period. Progressive hepatic fibrosis originating in the portal triads around occluded portal vein radicles occurred during the first year. Porto-systemic venous collaterals developed at the earliest three to four weeks after initial embolization. Angiographic changes included an increase in number and diameters of opacified hepatic arterial branches and a more dense arterial hepatogram than on the baseline studies, but these were only evident in advanced hepatic fibrosis. Decreases in portal and total hepatic blood flow of 53 +/- 15% and 17 +/- 7%, respectively, were observed after development of periportal fibrosis and stable portal hypertension, while the compensatory increase in hepatic arterial flow was a slowly evolving process resulting in an increase of 135 +/- 51% in the fibrotic stage. Animals with advanced hepatic fibrosis and portal hypertension remained in good general health, allowing extensive follow-up examinations at regular intervals over a prolonged period of time.