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Splanchnic vasodilation and hyperdynamic circulatory syndrome in cirrhosis.
World J Gastroenterol. 2014 Mar 14; 20(10):2555-63.WJ

Abstract

Portal hypertension is a clinical syndrome which leads to several clinical complications, such as the formation and rupture of esophageal and/or gastric varices, ascites, hepatic encephalopathy and hepato-renal syndrome. In cirrhosis, the primary cause of the increase in portal pressure is the enhanced resistance to portal outflow. However, also an increase in splanchnic blood flow worsens and maintains portal hypertension. The vasodilatation of arterial splanchnic vessels and the opening of collateral circulation are the determinants of the increased splanchnic blood flow. Several vasoactive systems/substances, such as nitric oxide, cyclooxygenase-derivatives, carbon monoxide and endogenous cannabinoids are activated in portal hypertension and are responsible for the marked splanchnic vasodilatation. Moreover, an impaired reactivity to vasoconstrictor systems, such as the sympathetic nervous system, vasopressin, angiotensin II and endothelin-1, plays a role in this process. The opening of collateral circulation occurs through the reperfusion and dilatation of preexisting vessels, but also through the generation of new vessels. Splanchnic vasodilatation leads to the onset of the hyperdynamic circulatory syndrome, a syndrome which occurs in patients with portal hypertension and is characterized by increased cardiac output and heart rate, and decreased systemic vascular resistance with low arterial blood pressure. Understanding the pathophysiology of splanchnic vasodilatation and hyperdynamic circulatory syndrome is mandatory for the prevention and treatment of portal hypertension and its severe complications.

Authors+Show Affiliations

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.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.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.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.

Pub Type(s)

Journal Article
Review

Language

eng

PubMed ID

24627591

Citation

Bolognesi, Massimo, et al. "Splanchnic Vasodilation and Hyperdynamic Circulatory Syndrome in Cirrhosis." World Journal of Gastroenterology, vol. 20, no. 10, 2014, pp. 2555-63.
Bolognesi M, Di Pascoli M, Verardo A, et al. Splanchnic vasodilation and hyperdynamic circulatory syndrome in cirrhosis. World J Gastroenterol. 2014;20(10):2555-63.
Bolognesi, M., Di Pascoli, M., Verardo, A., & Gatta, A. (2014). Splanchnic vasodilation and hyperdynamic circulatory syndrome in cirrhosis. World Journal of Gastroenterology, 20(10), 2555-63. https://doi.org/10.3748/wjg.v20.i10.2555
Bolognesi M, et al. Splanchnic Vasodilation and Hyperdynamic Circulatory Syndrome in Cirrhosis. World J Gastroenterol. 2014 Mar 14;20(10):2555-63. PubMed PMID: 24627591.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Splanchnic vasodilation and hyperdynamic circulatory syndrome in cirrhosis. AU - Bolognesi,Massimo, AU - Di Pascoli,Marco, AU - Verardo,Alberto, AU - Gatta,Angelo, PY - 2013/10/10/received PY - 2013/11/08/revised PY - 2013/11/28/accepted PY - 2014/3/15/entrez PY - 2014/3/15/pubmed PY - 2015/4/7/medline KW - Autonomic dysfunction KW - Cirrhosis KW - Hyperdynamic circulatory syndrome KW - Nitric oxide KW - Portal hypertension KW - Splanchnic flow KW - Splenic circulation SP - 2555 EP - 63 JF - World journal of gastroenterology JO - World J Gastroenterol VL - 20 IS - 10 N2 - Portal hypertension is a clinical syndrome which leads to several clinical complications, such as the formation and rupture of esophageal and/or gastric varices, ascites, hepatic encephalopathy and hepato-renal syndrome. In cirrhosis, the primary cause of the increase in portal pressure is the enhanced resistance to portal outflow. However, also an increase in splanchnic blood flow worsens and maintains portal hypertension. The vasodilatation of arterial splanchnic vessels and the opening of collateral circulation are the determinants of the increased splanchnic blood flow. Several vasoactive systems/substances, such as nitric oxide, cyclooxygenase-derivatives, carbon monoxide and endogenous cannabinoids are activated in portal hypertension and are responsible for the marked splanchnic vasodilatation. Moreover, an impaired reactivity to vasoconstrictor systems, such as the sympathetic nervous system, vasopressin, angiotensin II and endothelin-1, plays a role in this process. The opening of collateral circulation occurs through the reperfusion and dilatation of preexisting vessels, but also through the generation of new vessels. Splanchnic vasodilatation leads to the onset of the hyperdynamic circulatory syndrome, a syndrome which occurs in patients with portal hypertension and is characterized by increased cardiac output and heart rate, and decreased systemic vascular resistance with low arterial blood pressure. Understanding the pathophysiology of splanchnic vasodilatation and hyperdynamic circulatory syndrome is mandatory for the prevention and treatment of portal hypertension and its severe complications. SN - 2219-2840 UR - https://www.unboundmedicine.com/medline/citation/24627591/Splanchnic_vasodilation_and_hyperdynamic_circulatory_syndrome_in_cirrhosis_ L2 - https://www.wjgnet.com/1007-9327/full/v20/i10/2555.htm DB - PRIME DP - Unbound Medicine ER -