Copyright ©2010 Baishideng. All rights reserved.
World J Hepatol. Jun 27, 2010; 2(6): 208-220
Published online Jun 27, 2010. doi: 10.4254/wjh.v2.i6.208
Physiopathology of splanchnic vasodilation in portal hypertension
María Martell, Mar Coll, Nahia Ezkurdia, Imma Raurell, Joan Genescà
María Martell, Mar Coll, Nahia Ezkurdia, Imma Raurell, Joan Genescà, Liver Diseases Laboratory, Liver Unit, Department of Internal Medicine, Hospital Universitari Vall d’Hebron, Institut de Recerca, Universitat Autònoma de Barcelona, Barcelona 08035, Spain
Author contributions: Martell M, Coll M, Ezkurdia N and Raurell I drafted the various sections of the manuscript and made figures and illustrations; and Genescà J did the original design and approved the final version of the paper.
Supported by the Grants from the Ministerio de Educación y Ciencia, No. SAF2006-0314, and from the Ministerio de Ciencia e Innovación, No. SAF2009-08354
Correspondence to: Maria Martell, PhD, Liver Diseases Laboratory p006, Institut de Recerca Hospital Vall d’Hebron, Pg Vall d’Hebron 119-129, Barcelona 08035, Spain.
Telephone: +34-93-4894034 Fax: +34-93-4894032
Received: January 14, 2010
Revised: June 9, 2010
Accepted: June 16, 2010
Published online: June 27, 2010

In liver cirrhosis, the circulatory hemodynamic alterations of portal hypertension significantly contribute to many of the clinical manifestations of the disease. In the physiopathology of this vascular alteration, mesenteric splanchnic vasodilation plays an essential role by initiating the hemodynamic process. Numerous studies performed in cirrhotic patients and animal models have shown that this splanchnic vasodilation is the result of an important increase in local and systemic vasodilators and the presence of a splanchnic vascular hyporesponsiveness to vasoconstrictors. Among the molecules and factors known to be potentially involved in this arterial vasodilation, nitric oxide seems to have a crucial role in the physiopathology of this vascular alteration. However, none of the wide variety of mediators can be described as solely responsible, since this phenomenon is multifactorial in origin. Moreover, angiogenesis and vascular remodeling processes also seem to play a role. Finally, the sympathetic nervous system is thought to be involved in the pathogenesis of the hyperdynamic circulation associated with portal hypertension, although the nature and extent of its role is not completely understood. In this review, we discuss the different mechanisms known to contribute to this complex phenomenon.

Keywords: Liver cirrhosis, Portal hypertension, Splanchnic vasodilation, Hyperdynamic circulation, Sympathetic nervous system