Renal sodium retention and ascites formation in dogs with experimental cirrhosis but without portal hypertension or increased splanchnic vascular capacity.

Renal handling of sodium was studied in five dogs where an end-to-side portacaval fistula was constructed prior to the induction of cirrhosis with DMN. Such a model permits the effects of cirrhosis to be studied separately from the consequences of portal hypertension. Three control animals without cirrhosis maintained normal liver and kidney function and remained in sodium balance for as long as 8 weeks following surgery. In the five cirrhotic dogs, urinary sodium retention preceded ascites formation and was independent of hyperaldosteronism, hypoalbuminemia, hepatic ischemia, or decreased renal perfusion. Portal venous pressure remained normal in all cirrhotic dogs, and the splanchnic area remained free of venous collaterals. Plasma volume expansion also preceded ascites formation, and this variable increased by 8.4% (p less than 0.05) following 6 days of sodium retention. These temporal relationships between sodium retention, expanded plasma volume, and ascites formation are similar to those observed in ordinary cirrhotic dogs previously studied in this laboratory. Total plasma volume increased by 13.2% (p less than 0.05) when measured during the ascitic phase of cirrhosis. However, when the splanchnic and nonsplanchnic ("effective") components of plasma volume were measured by an exclusion technique, the ratio of these components to total plasma volume was not different from that observed in normal dogs. Thus no preferential consignment of retained salt and water had occurred. We conclude that urinary sodium retention in cirrhotic dogs occurs independently of portal hypertension or augmented splanchnic vascular capacity and is associated with expansion of the effective plasma volume, even though ascites is present.