Document Detail


Nitric oxide and portal hypertension.
MedLine Citation:
PMID:  12602508     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
In liver cirrhosis, an increase in hepatic resistance is the initial phenomenon leading to portal hypertension. This is primarily due to the structural distortion of the intrahepatic microcirculation caused by cirrhosis. However, similar to other vascular conditions, architectural changes in the liver are associated with a deficient nitric oxide (NO) production, which results in an increased vascular tone with a further increase in hepatic resistance and portal pressure. New therapeutic strategies are being developed to selectively provide the liver with NO, overcoming the deleterious effects of systemic vasodilators. On the other hand, a strikingly opposite process occurs in splanchnic arterial circulation, where NO production is increased. This results in splanchnic vasodilatation and subsequent increase in portal inflow, which contributes to portal hypertension. Systemic blockade of NO in portal hypertension attenuates the hyperdynamic circulation, but its effects increasing hepatic resistance may offset the benefit of reducing portal inflow, thus preventing an effective reduction of portal pressure. Moreover, it cannot be ruled out that NO blockade may have a deleterious action on cirrhosis progression, which raises caution about their use in patients with cirrhosis.
Authors:
Juan González-Abraldes; Juan Carlos García-Pagán; Jaime Bosch
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't; Review    
Journal Detail:
Title:  Metabolic brain disease     Volume:  17     ISSN:  0885-7490     ISO Abbreviation:  Metab Brain Dis     Publication Date:  2002 Dec 
Date Detail:
Created Date:  2003-02-26     Completed Date:  2003-07-03     Revised Date:  2006-11-15    
Medline Journal Info:
Nlm Unique ID:  8610370     Medline TA:  Metab Brain Dis     Country:  United States    
Other Details:
Languages:  eng     Pagination:  311-24     Citation Subset:  IM    
Affiliation:
Hepatic Hemodynamic Laboratory, Liver Unit, Hospital Clinic, IDIBAPS, University of Barcelona, Spain.
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MeSH Terms
Descriptor/Qualifier:
Animals
Collateral Circulation
Humans
Hypertension, Portal / drug therapy,  physiopathology*
Liver Cirrhosis / physiopathology
Nitric Oxide / antagonists & inhibitors,  metabolism*
Nitric Oxide Donors / therapeutic use
Portal System / physiopathology
Splanchnic Circulation
Vascular Resistance
Vasodilation
Chemical
Reg. No./Substance:
0/Nitric Oxide Donors; 10102-43-9/Nitric Oxide

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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