Patients with advanced cirrhosis show an abnormal regulation of extracellular fluid volume, resulting in the accumulation of fluid as ascites or edema. As portal hypertension develops, splanchnic arterial vasodilation also does due mainly to the production of nitric oxide (NO). Splanchnic arterial vasodilation decreases effective arterial blood volume, leading to fluid accumulation and renal function abnormalities which are a consequence of the homeostatic activation of vasoconstrictor and antinatriuretic factors. And the net effect is retention of sodium and water as well as renal vasoconstriction. The portal hypertension and splanchnic hyperdynamic circulation elevate the pressure of the splanchnic capillary circulation, leading to the accumulation of retained fluid as ascites.

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