Hemodynamic Changes in Splanchnic Blood Vessels in Portal Hypertension
Article first published online: 16 MAY 2008
Copyright © 2008 Wiley-Liss, Inc.
The Anatomical Record
Volume 291, Issue 6, pages 699–713, June 2008
How to Cite
Colle, I., Geerts, A. M., Van Steenkiste, C. and Van Vlierberghe, H. (2008), Hemodynamic Changes in Splanchnic Blood Vessels in Portal Hypertension. Anat Rec, 291: 699–713. doi: 10.1002/ar.20667
- Issue published online: 16 MAY 2008
- Article first published online: 16 MAY 2008
- Manuscript Accepted: 19 DEC 2007
- Manuscript Received: 14 MAY 2007
- portal hypertension;
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. Anat Rec, 291:699–713, 2008. © 2008 Wiley-Liss, Inc.