Pathophysiology of portal hypertension

Abstract

Portal hypertension is a major complication of liver disease that results from a variety of pathologic conditions that increase the resistance to the portal blood flow into the liver. As portal hypertension develops, the formation of collateral vessels and arterial vasodilation progresses, which results in increased blood flow to the portal circulation. Hyperdynamic circulatory syndrome develops, leading to esophageal varices or ascites. This article summarizes the factors that increase (1) intrahepatic vascular resistance and (2) the blood flow in the splanchnic and systemic circulations in liver cirrhosis. In addition, the future directions of basic/clinical research in portal hypertension are discussed.

Keywords: Cirrhosis; Fibrosis; Hyperdynamic circulation; Lymphatic system; Nitric oxide; Splenomegaly.

Copyright © 2014 Elsevier Inc. All rights reserved.

Figures

Figure 1

Portal hypertension leads to the development of the hyperdynamic circulatory syndrome, characterized by decreased mean arterial pressure (MAP), decreased systemic vascular resistance (SVR) and increased cardiac index (CI).

Figure 2. Activated hepatic stellate cells (HSCs) in liver cirrhosis increase intrahepatic vascular resistance

Quiescent HSCs are vitamin A storage cells and found in normal livers. In response to fibrogenic stimuli, such as transforming growth factor beta, HSCs are activated to become myofibroblasts, which exhibit a contractile and fibrogenic (collagen-producing) phenotype. These activated HSCs, located underneath liver sinusoidal endothelial cells, exert a contractile effect on the hepatic microcirculation, resulting in an increase in intrahepatic resistance.