Splanchnic hemodynamics in portal hypertensive dogs with portal fibrosis.

Splanchnic hemodynamics and portal systemic shunting were measured in eight dogs with experimentally induced portal fibrosis and splenomegaly and in six normal dogs by the radioactive microsphere technique. Portal fibrosis and splenomegaly were produced by repeated intraportal injections of a mixture of killed nonpathogenic Escherichia coli and dog anti-E. coli serum. All E. coli-treated dogs developed intrahepatic presinusoidal portal hypertension (portal vein pressure 15.8 +/- 5.4 vs. 7.5 +/- 0.9 mmHg in controls, P less than 0.005; intrahepatic pressure 6.8 +/- 2.1 vs. 6.2 +/- 1.4 mmHg in controls, NS) within 2.5 mo, but no portal systemic shunt was demonstrated at this time (2.1 +/- 1.5 vs. 0.7 +/- 0.4%, NS). Portal venous inflow, the total blood flow within the portal system, was increased in the treated dogs (27.6 +/- 6.6 vs. 18.2 +/- 2.5 ml X min-1 X kg body wt-1, P less than 0.005). Total splanchnic arterial vascular resistance was reduced in these dogs (26.0 +/- 10.4 vs. 40.9 +/- 4.6 dyn X s X cm-5 X 10(3), P less than 0.01) as a result of reduced arteriolar resistance in the spleen, jejunum and ileum, colon, and omentum, in all of which blood flow increased. In these animals both portal venous flow (27.0 +/- 6.5 vs. 18.1 +/- 2.5 ml X min-1 X kg body wt-1, P less than 0.005) and intrahepatic portal vascular resistance (1.9 +/- 0.7 vs. 0.7 +/- 0.3 dyn X s X cm-5 X 10(3), P less than 0.005) were increased.(ABSTRACT TRUNCATED AT 250 WORDS)