Molecular Mechanisms of Systemic Vasodilation and Hyperdynamic Circulatory State of Cirrhosis

Moreau, Richard; Lebrec, Didier

doi:10.1007/978-1-59259-885-4_4

Cited by 3 publications

(3 citation statements)

References 105 publications

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“…In portal hypertension, despite NOS and COX inhibition, arterial vasodilation, and vascular hyporeactivity are not totally suppressed, suggesting the presence of NOS/COX independent vasodilators (Moreau and Lebrec,1995). Increased plasma levels of natriuretic peptides, glucagon, adrenomedulin, calcitonin gene‐related peptide, substance P, and vasoactive intestinal peptide have been described in cirrhosis (Moreau and Lebrec,1995,2005). Probably, other vasodilators will be discovered in the future…”

Section: Mechanism Of Splanchnic Hyperdynamic Circulationmentioning

confidence: 99%

“…In normal circumstances NO stimulates the production of cGMP which activates cGMP dependent serine‐threonine protein kinase called “PKG” (Lincoln and Cornwell,1993). PKG inhibits the GPCR signaling pathway used by vasoconstrictors at different levels: (1) PKG increases GTPase activity terminating vasoconstrictor signalling (Tang et al,2003); (2) PKG may phosphorylate GPCR and thus uncouple the receptor and G‐proteins (Lincoln and Cornwell,1993; Moreau and Lebrec,2005).…”

Section: Mechanism Of Splanchnic Hyperdynamic Circulationmentioning

confidence: 99%

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Hemodynamic Changes in Splanchnic Blood Vessels in Portal Hypertension

Colle

Geerts

Steenkiste

et al. 2008

The Anatomical Record

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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.

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Section: Mechanism Of Splanchnic Hyperdynamic Circulationmentioning

confidence: 99%

Section: Mechanism Of Splanchnic Hyperdynamic Circulationmentioning

confidence: 99%

Hemodynamic Changes in Splanchnic Blood Vessels in Portal Hypertension

Colle

Geerts

Steenkiste

et al. 2008

The Anatomical Record

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“…During the course of the disease, rising pressure differences lead to an increased risk of hepatic encephalopathy, hepatorenal syndrome, and the dreaded complication of acute variceal rupture. Unfortunately, once collaterals have developed, increased levels of circulating endogenous vasodilators that result from the underlying liver disease, can lead to further increases in portal venous flow, exacerbating the risk of variceal rupture and other complications (3).…”

mentioning

confidence: 99%

Four‐dimensional velocity mapping of the hepatic and splanchnic vasculature with radial sampling at 3 tesla: A feasibility study in portal hypertension

Frydrychowicz

Landgraf

Niespodzany

et al. 2011

Magnetic Resonance Imaging

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Purpose To demonstrate the feasibility of PC-VIPR (Phase Contrast Vastly undersampled Imaging with Projection Reconstruction) for the depiction and hemodynamic analysis of hepatic and splanchnic vessels in patients with portal hypertension. Methods & Materials 24 cirrhotic patients (55.9±10.4years) were scanned using 5-point PC-VIPR for high spatial resolution imaging with large volume coverage at 3T using a 32-channel body coil. Vessel segmentation and hemodynamic visualization included color-coded 3D streamlines and particle traces. Segmentation quality was compared to contrast-enhanced multi-phase liver imaging. Flow pattern analysis was performed in consensus of 3 readers. The MELD score was calculated to estimate disease severity and was correlated to image quality. Results Good to excellent visualization quality was achieved in 23/24 cases. All arterial vessels and 144/168 vessels of the portal venous (PV) circulation were unambiguously identified. No correlation with the MELD score was found. 8/148 vessels of the PV circulation demonstrated reverse (hepatofugal) flow. Hepatofugal flow small tributaries to PV flow were present in three cases despite hepatopetal flow in the PV. Conclusion This feasibility study demonstrates the feasibility of PC-VIPR for simultaneous morphological and hemodynamic assessment of the hepatic and splanchnic vasculature in cirrhosis and portal hypertension. Future studies with quantitative analyses are warranted.

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Molecular and Structural Basis of Portal Hypertension

Moreau

Lebrec

2006

Clinics in Liver Disease

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Molecular Mechanisms of Systemic Vasodilation and Hyperdynamic Circulatory State of Cirrhosis

Cited by 3 publications

References 105 publications

Hemodynamic Changes in Splanchnic Blood Vessels in Portal Hypertension

Hemodynamic Changes in Splanchnic Blood Vessels in Portal Hypertension

Four‐dimensional velocity mapping of the hepatic and splanchnic vasculature with radial sampling at 3 tesla: A feasibility study in portal hypertension

Molecular and Structural Basis of Portal Hypertension

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