RENAL SODIUM RETENTION AND ASCITES FORMATION IN DOGS WITH EXPERIMENTAL CIRRHOSIS BUT WITHOUT PORTAL-HYPERTENSION OR INCREASED SPLANCHNIC VASCULAR CAPACITY

Abstract

Renal handling of Na was studied in 5 dogs where an end-to-side portacaval fistula was constructed prior to the induction of cirrhosis with dimethylnitrosamine (DMN). Such a model permitted 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 Na balance for as long as 8 wk following surgery. In the 5 cirrhotic dogs, urinary Na 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 < 0.05) following 6 days of Na retention. These temporal relationships between Na 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 < 0.05) when measured during the ascitic phase of cirrhosis. 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. No preferential consignment of retained salt and H2O had occurred. Urinary Na retention in cirrhotic dogs occurred independently of portal hypertension or augmented splanchnic vascular capacity and was associated with expansion of the effective plasma volume, even though ascites was present.