Figure 230

Three theories of ascites formation in hepatic cirrhosis. Hepatic venous outflow obstruction leads to portal hypertension. According to the underfill theory, transudation from the liver leads to reduction of the blood volume, thereby stimulating sodium (Na) retention by the kidney. As indicated by the question mark near the term blood volume, a low blood volume is rarely detected in clinical or experimental cirrhosis. Furthermore, this theory predicts that ascites would develop before renal Na retention, when the reverse generally occurs. According to the overflow theory, increased portal pressure stimulates renal Na retention through incompletely defined mechanisms. As indicated by the question mark near the arrow from hepatic venous outflow obstruction to UNaV, the nature of the portal hypertension-induced signals for renal Na retention remains unclear. The vasodilation theory suggests that portal hypertension leads to vasodilation and relative arterial hypotension. Evidence for vasodilation in cirrhosis that precedes renal Na retention is now convincing, as shown in Figures 2-31 and 2-33 [63].

Vasodilators

Vasoconstrictors

Vasodilators

Vasoconstrictors

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