Recent advances in the pathophysiology of portal hypertension

Portal hypertension is a common complication of chronic liver disease. Increased resistance to portal blood flow through a cirrhotic liver initiates the development of portal hypertension. In addition, alteration of neural and humoral regulations, endothelins, and stellate cells all contribute to the increased intrahepatic resistance. Moreover, the collateral circulation represents an additional site of increased resistance to portal blood flow. Increased splanchnic blood flow appears to play an important role in the maintenance of chronic portal hypertension. Several mechanisms have been proposed to explain this haemodynamic derangement including increased circulating vasodilators, endothelial-derived vasodilators, and decreased vascular reactivity to vasoconstrictors. Finally, the development of portal hypertension induces peripheral arterial vasodilation. The arterial vasodilatation may result in an increase in vascular underfilling which in turn leads to sodium retention and plasma volume expansion. The increased plasma volume is necessary for the development of increased cardiac output and the full expression of hyperdynamic circulation in portal hypertension.