Dogs with experimental cirrhosis of the liver but without intrahepatic hypertension do not retain sodium or form ascites.

Abstract

A B S T R A C T Dogs with portal cirrhosis but without portal hypertension (end-to-side portacaval anastomosis) retain sodium and expand plasma volume before ascites formation. In our study, dogs were subjected to bile duct ligation and simultaneous side-toside portacaval anastomosis (PCA) in order to create a canine model of hepatic cirrhosis without intrahepatic or portal hypertension. The effect of normalizing intrahepatic pressures in the face of venous outflow block on sodium handling was studied. 13 dogs survived the surgical procedures and were followed. Two dogs developed sodium retention and ascites at 5-6 wk (livers were cirrhotic) when the PCA spontaneously closed. 11 dogs were free of sodium retention and ascites for as long as 12 wks after surgery, while ingesting 35 meq/d of sodium. In this group glomerular filtration rate remained normal throughout the period of observation and there was no expansion of plasma volume. Nine of these dogs were then fed 85 meq/d of sodium; eight remained in sodium balance and one retained sodium and went on to develop ascites. When 10-15 mg i.m. of desoxycorticosterone acetate (DOCA) was given daily, five dogs developed sodium retention and ascites, while four escaped from DOCA. Dogs who developed ascites had either a partially occluded PCA (4/5) or a patent PCA, but with a significant portacaval pressure gradient of 9.5 cm H20

Relationships between plasma atrial natriuretic peptide concentrations and hemodynamics and hematocrit in patients with cirrhosis

“…Because ANP infusion decreased wedged hepatic venous pressure in patients with cirrhosis (40), it is unlikely that increased plasma ANP concentrations contributed to high portal pressure in our study. On the other hand, it is possible that portal hypertension stimulated ANP release because portal hypertension per se may increase blood volume through enhanced sodium retention (36) and because hypervolemia stimulates ANP release (33-35).…”

Sympathetic Nervous Regulation in Patients with Cirrhosis: Pathogenesis of Fluid Retention and Formation of Ascites

“…Dogs with experimenta l cirrhosis, but without sinusoiJal hype rtension , do not retain soJ ium an d water (45).…”

Ascites Formation in Liver Cirrhosis: The How and the Why

“…Hepatoportal hypertension is an essential element in the hepatic ascites syndrome [3,12]. Different explanations of the portal hy pertension have been suggested, but most investigators agree on the concept of a postor late-sinusoidal obstruction, resulting in almost identical elevation of the pressures in the liver sinusoids and in the portal vein.…”

“…However, not only hydrostatic and oncotic pressures are in volved in the formation of ascites. The ele vated portal pressure bears a relation to im portant neurohumoral mechanisms, which play parts in a complex homeostatic process ultimately resulting in renal sodium and wa ter retention [12][13][14][15].…”