title: Sodium retention and ascites formation in dogs with experimental portal cirrhosis.
abstract: Experimental cirrhosis was produced in dogs by the sporadic feeding of dimethylnitrosamine for the purpose of studying the temporal relationships between urinary sodium retention, plasma volume expansion, and ascites formation. Sodium retention started about 16 days following the onset of cirrhosis and preceded ascites formation by about 10 days. Plasma volume increased by 9% (P less than 0.05) within 3-4 days of sodium retention and expanded further as ascites accumulated. Splanchnic plasma volume was greater by 161 ml in 10 cirrhotic dogs with ascites than in 14 normal dogs. Nonsplanchnic volume was greater by 96 ml (P less than 0.05). Thus, the "effective" as well as the splanchnic component of the vascular space was expanded. Paracentesis did not cause the re-formation of ascites in five dogs as long as dietary salt was denied. Refeeding permitted reaccumulation of ascites and further plasma volume expansion. Renal perfusion remained constant as dogs became progressively cirrhotic. We conclude that ascites formation depends on the prior retention of urinary sodium, and occurs as an "overflow" phenomenon. A contracted effective plasma volume does not appear to be necessary for continuing sodium retention.
mesh_terms: D000818:Animals; D001201:Ascites / Q000209:etiology*; D001810:Blood Volume; D002496:Central Venous Pressure; D003714:Denervation; D004128:Dimethylnitrosamine; D004285:Dogs; D007668:Kidney / Q000503:physiopathology*; D007684:Kidney Tubules / Q000503:physiopathology; D008106:Liver Cirrhosis, Experimental / Q000139:chemically induced / Q000150:complications / Q000503:physiopathology*; D009318:Natriuresis; D011168:Portal System / Q000503:physiopathology; D012964:Sodium / Q000378:metabolism* / Q000652:urine; D014690:Venous Pressure; D014882:Water-Electrolyte Balance
chemical_list: D012964:Sodium; D004128:Dimethylnitrosamine