title: Portal hypertension: from bedside to bench.
abstract: The initial factor leading to portal hypertension is an increase in hepatic resistance. Later, an increase in portal blood flow contributes to maintain and exacerbate portal hypertension despite the development of portosystemic collaterals. The critical step in the development and acceptance of these concepts, which proved crucial for the management of patients with portal hypertension, was the development of animal models. These allowed the full characterization of the profound hemodynamic abnormalities in the systemic and splanchnic circulation associated with portal hypertension, and the elucidation of the molecular mechanisms implicated in these disturbances. This review traces how seminal clinical observations in the 1950s raised meaningful questions that were subsequently answered at the bench, leading to our current understanding of the pathophysiology of portal hypertension and of the pathogenesis of severe complications of cirrhosis, such as variceal bleeding or ascites.
authors.affiliation: Veterans Administration Medical Center, West Haven, CT 06516, USA. roberto.groszmann@yale.edu
authors.forename: Roberto J
authors.initials: RJ
authors.lastname: Groszmann
authors.forename: Juan G
authors.initials: JG
authors.lastname: Abraldes
mesh_terms: D000818:Animals; D006439:Hemodynamics / Q000502:physiology; D006801:Humans; D006975:Hypertension, Portal / Q000209:etiology* / Q000503:physiopathology; D008102:Liver Circulation / Q000502:physiology; D008103:Liver Cirrhosis / Q000503:physiopathology; D009569:Nitric Oxide / Q000502:physiology; D011168:Portal System / Q000502:physiology; D013152:Splanchnic Circulation / Q000502:physiology; D014655:Vascular Resistance / Q000502:physiology
chemical_list: D009569:Nitric Oxide