Acute portal vein stenosis. An experimental study on portal circulation and hepatosplenic function

Portal hypertension was mechanically induced in rats by acute constriction of the portal vein. Using a new "button" technique, a stricture 0.9 mm in diameter was found to be compatible with life in more than 90% of the rats. Angiographic and anatomic studies of portosystemic collaterals confirmed observations in earlier experiments. Oesophageal varices were not seen, despite sustained elevation of portal venous pressure during the four weeks following induction of portal hypertension. Development of paraportal veins bridging the obstacle is suggested to be responsible for maintenance of normal liver structure and for recovery from the transient hepatic dysfunction. Increase of phagocytosis in the germinal centres of the enlarged spleens was found after four weeks, suggesting immunologic changes caused by portal hypertension and/or portosystemic shunt circulation.