Portal Hypertension

Bosch, Jaime; Navasa, Miquez; García-Pagán, J.C.; DeLacy, A.M.; Rodés, Joan

doi:10.1016/s0025-7125(16)30646-0

Cited by 87 publications

(45 citation statements)

References 77 publications

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“…Hemodynamic measurements were performed in fasting conditions as previously described [17,18]. Briefly, patients were placed in a supine position for at least 4 h before the study.…”

Section: Hemodynamicsmentioning

confidence: 99%

Hemodynamics and pharmacokinetics of tezosentan, a dual endothelin receptor antagonist, in patients with cirrhosis

Lebrec

Bosch

Jalan

et al. 2011

Eur J Clin Pharmacol

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“…Hemodynamic measurements were performed in fasting conditions as previously described [17,18]. Briefly, patients were placed in a supine position for at least 4 h before the study.…”

Section: Hemodynamicsmentioning

confidence: 99%

Hemodynamics and pharmacokinetics of tezosentan, a dual endothelin receptor antagonist, in patients with cirrhosis

Lebrec

Bosch

Jalan

et al. 2011

Eur J Clin Pharmacol

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“…Clinical consequences include hepatic encephalopathy and elevated hemorrhagic diathesis. Furthermore, the massive alterations in hepatic microcirculation caused by hepatic fi brosis are a major reason for further clinical complications such as portal hypertension, formation of esophageal, gastric or rectal varices with the risk of lifethreatening hemorrhage, portal hypertensive gastropathy, ascites, and hepatorenal syndrome [110] . The pathophysiological mechanism of these complications comprises the signifi cant diminution of overall vascular cross-sectional area.…”

Section: From Alcoholic Liver Fibrosis To Cirrhosisclinical Consequencesmentioning

confidence: 99%

Molecular Mechanisms of Alcohol-Induced Hepatic Fibrosis

Siegmund¹,

Dooley²,

Brenner³

2005

Dig Dis

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Alcohol abuse is a major cause of liver fibrosis and cirrhosis in developed countries. Before alcoholic liver fibrosis becomes evident, the liver undergoes several stages of alcoholic liver disease including steatosis and steatohepatitis. Although the main mechanisms of fibrogenesis are independent of the etiology of liver injury, alcoholic liver fibrosis is distinctively characterized by a pronounced inflammatory response due to elevated gut-derived endotoxin plasma levels, an augmented generation of oxidative stress with pericentral hepatic hypoxia and the formation of cell-toxic and profibrogenic ethanol metabolites (e.g. acetaldehyde or lipid oxidation products). These factors, based on a complex network of cytokine actions, together result in increased hepatocellular damage and activation of hepatic stellate cells, the key cell type of liver fibrogenesis. Although to date removal of the causative agent, i.e. alcohol, still represents the most effective intervention to prevent the manifestation of alcoholic liver disease, sophisticated molecular approaches are underway, aiming to specifically blunt profibrogenic signaling pathways in liver cells or specifically induce cell death in activated hepatic stellate cells to decrease the scarring of the liver.

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“…1 The splanchnic circulation is also hyperkinetic, with an increase in portal blood flow, which is an important factor in the development of portal hypertension. 2 Although the mechanism for the genesis of this hyperdynamic state is not well known, glucagon-3,4 and endothelial-derived factors 5,6 may be involved through their vasodilatory effects.…”

confidence: 99%

Splanchnic hyperemia after liver transplantation in patients with end-stage liver disease

et al. 1998

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Systemic and splanchnic hemodynamic parameters were evaluated in 12 patients with cirrhosis before and 3 and 6 months after liver transplantation. Results were compared with those obtained in 8 healthy subjects. Three months after liver transplantation recipients had an increase in mean arterial pressure (98 ؎ 7 v 78 ؎ 9 mmHg; P F .05), an insignificant decrease in cardiac index ; portal blood flow, 1,520 ؎ 180 mL/min). Systemic hemodynamics 6 months after liver transplantation were similar to those observed in the healthy control group (mean arterial pressure, 95 ؎ 6 mmHg; cardiac index, 2.9 ؎ 0.9 L · min ؊1 · m ؊2 ; peripheral vascular resistance, 1,480 ؎ 380 dyne · s · cm ؊5 ). However, portal blood flow was still significantly higher than in healthy controls at 6 months (1,520 ؎ 180 v 910 ؎ 140 mL/min; P F .05). This study shows that systemic hemodynamics are normalized after liver transplantation. However, an increase in portal blood flow occurs and persists for at least 6 months after liver transplantation. Further studies are needed to clarify the cause of the abnormally high portal flows.

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Portal Hypertension

Cited by 87 publications

References 77 publications

Hemodynamics and pharmacokinetics of tezosentan, a dual endothelin receptor antagonist, in patients with cirrhosis

Hemodynamics and pharmacokinetics of tezosentan, a dual endothelin receptor antagonist, in patients with cirrhosis

Molecular Mechanisms of Alcohol-Induced Hepatic Fibrosis

Splanchnic hyperemia after liver transplantation in patients with end-stage liver disease

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