Figure 230

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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

FIGURE 2-31

Alterations in cardiovascular hemodynamics in hepatic cirrhosis. Hepatic dysfunction and portal hypertension increase the production and impair the metabolism of several vasoac-tive substances. The overall balance of vasoconstriction and vasodilation shifts in favor of dilation. Vasodilation may also shift blood away from the central circulation toward the periphery and away from the kidneys. Some of the vasoactive substances postulated to participate in the hemodynamic disturbances of cirrhosis include those shown here. ANP—atrial natrivretic peptide; ET-1—endothelin-1; CGRP—calcitonin gene related peptide; RAAS—renin/angiotensin/aldosterone system; TNF—tumor necrosis factor; VIP— vasoactive intestinal peptide. (Data from Moller and Henriksen [64].)

Central blood volume

Noncentral blood volume

Central blood volume

Noncentral blood volume

Control subjects, n=16 Cirrhotic patients, n=60

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