ArticlePloS one2015
Hepatic arterial vasodilation is independent of portal hypertension in early stages of cirrhosis.
Article in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 18 citations in OpenAlex.
- Fetal Hepatic Circulation: From Vascular Physiology to Doppler Assessment.Diagnostics (Basel, Switzerland) · 2025Review
- Diffuse hepatic artery dilation: an uncommon manifestation of early cirrhosis.Oxford medical case reports · 2025Article
- Pharmacological Modulation of Liver and Spleen Stiffness in a Cirrhotic Rat Model.Hepatic medicine : evidence and research · 2025Article
- Eplerenone, a mineralocorticoid receptor inhibitor, reduces cirrhosis associated changes of hepatocyte glucose and lipid metabolism.Cell communication and signaling : CCS · 2024Article
- The selective mineralocorticoid receptor antagonist eplerenone prevents decompensation of the liver in cirrhosis.British journal of pharmacology · 2018Article
- Restructuring of the vascular bed in response to hemodynamic disturbances in portal hypertension.World journal of hepatology · 2016Review
- Does pressure cause liver cirrhosis? The sinusoidal pressure hypothesis.World journal of gastroenterology · 2016Article
- Increased Hepatic Arterial Blood Flow Measured by Hepatic Perfusion Index in Hepatosplenic Schistosomiasis: New Concepts for an Old Disease.Digestive diseases and sciences · 2016Article
- Thrombin activation and liver inflammation in advanced hepatitis C virus infection.World journal of gastroenterology · 2016Review
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
introductionThe compensatory increase in hepatic arterial flow with a decrease in portal venous flow is known as the hepatic arterial buffer response. In cirrhosis with elevated portal pressure, the vascular resistance of the hepatic artery is decreased. Whether this lower resistance of the hepatic artery is a consequence of portal hypertension or not remains unknown. STUDY
aimThe aim of the study was to investigate the hepatic arterial resistance and response to vasoconstriction in cirrhosis without portal hypertension (normal portal resistance).
methodsCirrhosis was induced by CCl4-inhalation for 8 weeks (8W, normal portal resistance) and for 12-14 weeks (12W, elevated portal resistance). Bivascular liver perfusion was performed at 8W or 12W and dose response curves of methoxamine were obtained in the presence or absence of LNMMA (nitric oxide synthase blocker). Vascular resistances of the hepatic artery (HAR), portal vein (PVR) and sinusoids (SVR) were measured. Western Blot (WB) and Immunohistochemistry (IHC) were done to measure eNOS and HIF 1a expression.
resultsHAR in both groups of cirrhotic animals (8W and 12W) were lower compared to controls. Dose response curves to methoxamine revealed lower HAR in both cirrhotic models (8W and 12W) regardless the magnitude of portal resistance. LNMMA corrected the dose response curves in cirrhosis (8W and 12W) to control. WB and IHC show increased protein expression of eNOS and HIF1a in 8W and 12W.
conclusionHepatic arterial resistance is decreased in cirrhosis independent of portal resistance. Vasodilation of the hepatic artery in cirrhosis seems to be influenced by hypoxia rather than increase in portal resistance. Nitric oxide is the main vasodilator.
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