Hepatic Regulation of Sodium and Water in Ascites

FACTORS INVOLVED in the production and maintenance of ascites secondary to cirrhosis of the liver are not clearly understood. Outflow obstruction of the hepatic veins, hypoproteinemia,¹ and hyperaldosteronism² have been implicated in its etiology. More recently, additional factors have been suggested to play a role in the formation of ascites. Baronofsky³ succeeded in ameliorating experimental ascites in dogs by thyroidectomy. He postulated a thyroid-adrenal interrelationship in the causation of cirrhotic ascites. Mittlemann⁴ reported two patients with ascites secondary to cirrhosis who had a naturesis in the face of rising urinary aldosterone following portacaval shunts. This seeming paradox has not been adequately explained. Watson⁵ has called attention to the possibility of a humoral agent released by the cirrhotic liver that could cause ascites. More recently, Wolfman and associates^6,7 have presented experimental evidence that dogs with portacaval shunts retain more sodium and water in response to