Hydrogen sulphide and the hyperdynamic circulation in cirrhosis: a hypothesis
- 1Department of Pharmacology, School of Medicine, Tehran University of Medical Sciences, Tehran, Iran
- 2The UCL Institute of Hepatology, Department of Medicine, Royal Free and University College Medical School, University College London, London, UK
- Correspondence to:
Professor K Moore
The UCL Institute of Hepatology, Royal Free and University College Medical School, University College London, Rowland Hill St, London NW3 2PF, UK; kmooremedsch.ucl.ac.uk
- Accepted 20 July 2005
- Revised 14 July 2005
- Published Online First 20 September 2005
Abstract
Cirrhosis is associated with the development of a hyperdynamic circulation, which is secondary to the presence of systemic vasodilatation. Several mechanisms have been postulated to be involved in the development of systemic vasodilatation, including increased synthesis of nitric oxide, hyperglucagonaemia, increased carbon monoxide synthesis, and activation of KATP channels in vascular smooth muscle cells in the systemic and splanchnic arterial circulation. 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 this brief review, we comment on what is known about H2S, vascular and neurological function, and postulate its role in the pathogenesis of the vascular abnormalities in cirrhosis.
Footnotes
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Conflict of interest: None declared.
