Copyright
©2014 Baishideng Publishing Group Co., Limited. All rights reserved.
World J Gastroenterol. Mar 14, 2014; 20(10): 2555-2563
Published online Mar 14, 2014. doi: 10.3748/wjg.v20.i10.2555
Published online Mar 14, 2014. doi: 10.3748/wjg.v20.i10.2555
Splanchnic vasodilation and hyperdynamic circulatory syndrome in cirrhosis
Massimo Bolognesi, Marco Di Pascoli, Alberto Verardo, Angelo Gatta, Department of Internal Medicine-DIMED, University of Padua, Azienda Ospedaliera Università di Padova, 35128 Padova, Italy
Author contributions: All authors contributed equally to this work.
Correspondence to: Massimo Bolognesi, MD, PhD, Department of Internal Medicine-DIMED, University of Padua, Azienda Ospedaliera Università di Padova, Clinica Medica 5, Via Giustiniani 2, 35128 Padova, Italy. massimo.bolognesi@unipd.it
Telephone: +39-49-8212383 Fax: +39-49-8754179
Received: October 10, 2013
Revised: November 8, 2013
Accepted: November 28, 2013
Published online: March 14, 2014
Processing time: 152 Days and 21.6 Hours
Revised: November 8, 2013
Accepted: November 28, 2013
Published online: March 14, 2014
Processing time: 152 Days and 21.6 Hours
Core Tip
Core tip: In cirrhosis, portal hypertension is due to an increase in intrahepatic resistance and splanchnic blood flow. The latter is secondary to arterial splanchnic vasodilatation and the opening of collateral circulation. Though the increase in intrahepatic resistance is the earliest and most important component, at present the only treatment regimes which are available for the control of portal hypertension in cirrhosis, i.e., non-selective beta-blockers, octreotide and terlipressin, act on the splanchnic dynamic component. Thus, understanding the mechanisms that lead to splanchnic vasodilatation and to the hyperdynamic circulatory syndrome is essential for the treatment of the complications of portal hypertension.