The definitive surgical treatment of portal hypertension secondary to cirrhosis of the liver is intended to lower portal venous pressure and thus prevent hemorrhage from collateral venous channels, usually esophageal varices. Various clinically successful procedures have been developed to shunt the portal blood around the obstructing hepatic vascular bed.1 A disadvantage of the shunting procedures currently in use is the deleterious effect on hepatic function that may follow a reduction in blood supply to the liver. This has been demonstrated experimentally in dogs with Eck fistulas.2,3 Deterioration of hepatic function has also been observed in some patients following portacaval shunt.4,5 By some authors it has been considered problematical whether this hepatic dysfunction might be due to diminution in the total blood supply or simply to diversion of the portal blood.
Silen et al.6 have shown that dogs with a surgical transposition of the portal vein and