Document Detail


Hemodynamic changes in splanchnic blood vessels in portal hypertension.
MedLine Citation:
PMID:  18484617     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Portal hypertension (PHT) is associated with a hyperdynamic state characterized by a high cardiac output, increased total blood volume, and a decreased splanchnic vascular resistance. This splanchnic vasodilation is a result of an important increase in local and systemic vasodilators (nitric oxide, carbon monoxide, prostacyclin, endocannabinoids, and so on), the presence of a splanchnic vascular hyporesponsiveness toward vasoconstrictors, and the development of mesenteric angiogenesis. All these mechanisms will be discussed in this review. To decompress the portal circulation in PHT, portosystemic collaterals will develop. The presence of these portosystemic shunts are responsible for major complications of PHT, namely bleeding from gastrointestinal varices, encephalopathy, and sepsis. Until recently, it was accepted that the formation of collaterals was due to opening of preexisting vascular channels, however, recent data suggest also the role of vascular remodeling and angiogenesis. These points are also discussed in detail.
Authors:
Isabelle Colle; Anja M Geerts; Christophe Van Steenkiste; Hans Van Vlierberghe
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Publication Detail:
Type:  Journal Article; Review    
Journal Detail:
Title:  Anatomical record (Hoboken, N.J. : 2007)     Volume:  291     ISSN:  1932-8494     ISO Abbreviation:  Anat Rec (Hoboken)     Publication Date:  2008 Jun 
Date Detail:
Created Date:  2008-05-22     Completed Date:  2008-06-27     Revised Date:  2009-12-16    
Medline Journal Info:
Nlm Unique ID:  101292775     Medline TA:  Anat Rec (Hoboken)     Country:  United States    
Other Details:
Languages:  eng     Pagination:  699-713     Citation Subset:  IM    
Affiliation:
Department of Hepatology and Gastroenterology, Ghent University Hospital, Ghent, Belgium. isabelle.colle@ugent.be
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MeSH Terms
Descriptor/Qualifier:
Animals
Biological Factors / physiology
Carbon Monoxide / physiology
Collateral Circulation / physiology
Endocannabinoids / physiology
Epoprostenol / physiology
Hemodynamics
Humans
Hypertension, Portal / etiology,  pathology,  physiopathology*
Liver Circulation / physiology
Models, Cardiovascular
Neovascularization, Pathologic
Nitric Oxide / physiology
Splanchnic Circulation / physiology*
Vascular Endothelial Growth Factor A / physiology
Vasodilation / physiology
Chemical
Reg. No./Substance:
0/Biological Factors; 0/Endocannabinoids; 0/Vascular Endothelial Growth Factor A; 0/endothelium-dependent hyperpolarization factor; 10102-43-9/Nitric Oxide; 35121-78-9/Epoprostenol; 630-08-0/Carbon Monoxide

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


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