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Hemodynamic changes in splanchnic blood vessels in portal hypertension.
Anat Rec (Hoboken). 2008 Jun; 291(6):699-713.AR

Abstract

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+Show Affiliations

Department of Hepatology and Gastroenterology, Ghent University Hospital, Ghent, Belgium. isabelle.colle@ugent.beNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Review

Language

eng

PubMed ID

18484617

Citation

Colle, Isabelle, et al. "Hemodynamic Changes in Splanchnic Blood Vessels in Portal Hypertension." Anatomical Record (Hoboken, N.J. : 2007), vol. 291, no. 6, 2008, pp. 699-713.
Colle I, Geerts AM, Van Steenkiste C, et al. Hemodynamic changes in splanchnic blood vessels in portal hypertension. Anat Rec (Hoboken). 2008;291(6):699-713.
Colle, I., Geerts, A. M., Van Steenkiste, C., & Van Vlierberghe, H. (2008). Hemodynamic changes in splanchnic blood vessels in portal hypertension. Anatomical Record (Hoboken, N.J. : 2007), 291(6), 699-713. https://doi.org/10.1002/ar.20667
Colle I, et al. Hemodynamic Changes in Splanchnic Blood Vessels in Portal Hypertension. Anat Rec (Hoboken). 2008;291(6):699-713. PubMed PMID: 18484617.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Hemodynamic changes in splanchnic blood vessels in portal hypertension. AU - Colle,Isabelle, AU - Geerts,Anja M, AU - Van Steenkiste,Christophe, AU - Van Vlierberghe,Hans, PY - 2008/5/20/pubmed PY - 2008/6/28/medline PY - 2008/5/20/entrez SP - 699 EP - 713 JF - Anatomical record (Hoboken, N.J. : 2007) JO - Anat Rec (Hoboken) VL - 291 IS - 6 N2 - 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. SN - 1932-8494 UR - https://www.unboundmedicine.com/medline/citation/18484617/Hemodynamic_changes_in_splanchnic_blood_vessels_in_portal_hypertension_ L2 - https://doi.org/10.1002/ar.20667 DB - PRIME DP - Unbound Medicine ER -