Abstract
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,<sup>1</sup>and hyperaldosteronism<sup>2</sup>have been implicated in its etiology. More recently, additional factors have been suggested to play a role in the formation of ascites. Baronofsky<sup>3</sup>succeeded in ameliorating experimental ascites in dogs by thyroidectomy. He postulated a thyroid-adrenal interrelationship in the causation of cirrhotic ascites. Mittlemann<sup>4</sup>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. Watson<sup>5</sup>has called attention to the possibility of a humoral agent released by the cirrhotic liver that could cause ascites. More recently, Wolfman and associates<sup>6,7</sup>have presented experimental evidence that dogs with portacaval shunts retain more sodium and water in response to
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