Hyperdynamic circulation in cirrhosis: a role for nitric oxide?

@article{Vallance1991HyperdynamicCI,
  title={Hyperdynamic circulation in cirrhosis: a role for nitric oxide?},
  author={Patrick Vallance and Salvador Moncada},
  journal={The Lancet},
  year={1991},
  volume={337},
  pages={776-778}
}
Nitric oxide as a mediator of hemodynamic abnormalities and sodium and water retention in cirrhosis.
TLDR
Evidence is provided suggesting that nitric oxide has an important role in the hemodynamic abnormalities that characterize cirrhosis and the associated sodium and water.
Hydrogen sulphide and the hyperdynamic circulation in cirrhosis: a hypothesis
TLDR
Hydrogen sulphide (H2S) has recently been identified as a novel gaseous transmitter that induces vasodilatation through activation of KATP channels in vascular smooth muscle cells in the systemic and splanchnic arterial circulation.
Nitric oxide and the hyperdynamic circulation in cirrhosis: is there a role for selective intestinal decontamination?
TLDR
The proposal that endotoxaemia, possibly from gut-derived bacterial translocation, causes induction of NOS (NO synthase) leading to increased vascular NO production, which is the primary stimulus for the development of vasodilatation in cirrhosis and its accompanying clinical manifestations is focused on.
Increased Nitric Oxide in the Exhaled Air of Patients with Decompensated Liver Cirrhosis
TLDR
Patients with liver cirrhosis often present with several systemic hemodynamic disturbances, including hypotension, low systemic vascular resistance, and a reduced sensitivity to vasoconstrictors, so the hypothesis that an increased synthesis and release of nitric oxide accounts for hemodynamic abnormalities in patients with liver Cirrhosis was investigated.
Cardiovascular Abnormalities in Cirrhosis: the Possible Mechanisms
TLDR
The major mechanisms that may underlie cirrhosis are examined, concentrating on nitric oxide, endocannabinoids, prostaglandins, carbon monoxide, endogenous opioids, and adrenergic receptor changes.
Hemodynamic alterations in liver cirrhosis.
Nitric-oxide-lowering effect of terlipressin in decompensated cirrhosis: comparison to the molecular adsorbent recirculating system and correlation with clinical status
TLDR
The findings suggest that terlipressin may be the vasopressor agent of choice in patients with decompensated cirrhosis and provide a rationale for combination ter Lipressin and MARS therapy when the therapeutic response to either treatment alone is suboptimal.
Current pharmacotherapy in the management of cirrhosis: focus on the hyperdynamic circulation
Many major complications of hepatic cirrhosis relate to the development of a characteristic hyperdynamic circulatory state in these patients, irrespective of the underlying disease aetiology.
Portal hypertension and cirrhosis: the role of inflammation and nitric oxide.
TLDR
Evidence is provided for significantly elevated portal pressure in alcoholic hepatitis patients, who were shown to have a marked additional inflammatory response on the background of cirrhosis, and a more severe expression of disease.
...
1
2
3
4
5
...

References

SHOWING 1-10 OF 21 REFERENCES
Role of endothelium-derived relaxing factor in regulation of renal hemodynamic responses.
TLDR
Treatment with NG-monomethyl-L-arginine (L-NMMA), an inhibitor of enzymatic synthesis of nitric oxide from L- arginine, prevented the ACh-induced increase in urinary cGMP excretion as well as the systemic and renal hemodynamic effects of ACh.
Loss of vascular responsiveness induced by endotoxin involves L-arginine pathway.
TLDR
Results demonstrate that activation of the L-arginine pathway has a major role in the production of vascular hyporeactivity in endotoxemia, ex vivo as well as in vivo, and suggest that endothelium-independent vascular production of NO may be involved.
The acute splanchnic and peripheral tissue metabolic response to endotoxin in humans.
TLDR
The in vivo alterations in organ-specific substrate processing and endogenous mediator production induced by endotoxin were investigated in healthy volunteers and the net cachectin efflux from the splanchnic organs demonstrates that these tissues are a major site for production of this cytokine.
The cardiovascular response of normal humans to the administration of endotoxin.
TLDR
It is concluded that the administration of endotoxin to normal subjects causes a depression ofleft ventricular function that is independent of changes in left ventricular volume or vascular resistance, and suggests that endotoxin is a major mediator of the cardiovascular dysfunction in this condition.
Role of endothelium-derived nitric oxide in the regulation of blood pressure.
  • D. Rees, R. Palmer, S. Moncada
  • Biology, Medicine
    Proceedings of the National Academy of Sciences of the United States of America
  • 1989
TLDR
Results indicate that nitric oxide formation from L-arginine by the vascular endothelium plays a role in the regulation of blood pressure and in the hypotensive actions of acetylcholine.
...
1
2
3
...