Effects of portacaval shunt, transposition, and dimethylnitrosamine-induced chronic liver injury on pancreatic hormones and amino acids in dog.

The effect of portacaval shunt on amino acid metabolism and pancreatic hormone secretion remains a subject of controversy. This might be due to the fact that shunt has two consequences; it shunts portal blood into the systemic circulation, and it causes hepatic parenchyma dysfunction by decreasing total hepatic blood flow. In order to see which one of these two is the more important factor, we created a model of portacaval transposition in dogs (PCT) causing portal systemic shunting without impairing hepatic blood flow and compared it with a model of hepatic dysfunction in dogs created by administering dimethylnitrosamine (DMNA). The dynamics of amino acid levels and pancreatic hormone secretion in the portal blood were investigated. DMNA dogs and dogs with a standard end-to-side portacaval shunt (Eck) showed elevated immunoreactive glucagon (IRG) levels and low immunoreactive insulin (IRI) levels in the portal blood as well as an amino acid imbalance, while values in PCT dogs were similar to those of controls. These data suggested that high IRG and low IRI in the portal blood and amino acid disturbances in the dogs with Eck shunts were due to hepatic parenchyma dysfunction, rather than to portal-systemic shunting.