title: Splanchnic vasodilation and hyperdynamic circulatory syndrome in cirrhosis.
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.affiliation: 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.
authors.forename: Massimo
authors.initials: M
authors.lastname: Bolognesi
authors.affiliation: 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.
authors.forename: Marco
authors.initials: M
authors.lastname: Di Pascoli
authors.affiliation: 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.
authors.forename: Alberto
authors.initials: A
authors.lastname: Verardo
authors.affiliation: 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.
authors.forename: Angelo
authors.initials: A
authors.lastname: Gatta
mesh_terms: D000818:Animals; D062186:Arterial Pressure; D002302:Cardiac Output; D003097:Collateral Circulation; D006339:Heart Rate; D006801:Humans; D006975:Hypertension, Portal / Q000188:drug therapy / Q000209:etiology* / Q000378:metabolism / Q000503:physiopathology; D018836:Inflammation Mediators / Q000378:metabolism; D008103:Liver Cirrhosis / Q000150:complications* / Q000378:metabolism / Q000503:physiopathology; D017082:Portal Pressure; D012039:Regional Blood Flow; D015398:Signal Transduction; D013152:Splanchnic Circulation / Q000187:drug effects; D013577:Syndrome; D014655:Vascular Resistance; D014662:Vasoconstrictor Agents / Q000627:therapeutic use; D014664:Vasodilation / Q000187:drug effects
chemical_list: D018836:Inflammation Mediators; D014662:Vasoconstrictor Agents
keywords: Autonomic dysfunction; Cirrhosis; Hyperdynamic circulatory syndrome; Nitric oxide; Portal hypertension; Splanchnic flow; Splenic circulation