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Hydrogen sulphide and the hyperdynamic circulation in cirrhosis: a hypothesis
M R Ebrahimkhani1, A R Mani, K Moore
1Department of Pharmacology, School of Medicine, Tehran University of Medical Sciences, Tehran, Iran.
Gut
|September 22, 2005
Summary
Hydrogen sulfide (H2S) may play a role in cirrhosis-related vascular issues. This gas transmitter induces vasodilation by activating K(ATP) channels, potentially contributing to the hyperdynamic circulation seen in liver cirrhosis.
Area of Science:
- Cardiovascular Physiology
- Gastroenterology
- Vascular Biology
Background:
- Cirrhosis causes a hyperdynamic circulation due to systemic vasodilation.
- Mechanisms include nitric oxide, hyperglucagonaemia, carbon monoxide, and K(ATP) channel activation.
- Vascular smooth muscle cells in systemic and splanchnic circulation are affected.
Purpose of the Study:
- To review the role of hydrogen sulfide (H2S) in vascular and neurological function.
- To postulate H2S's involvement in the vascular abnormalities of cirrhosis.
Main Methods:
- Literature review of existing studies on H2S and vascular function.
- Analysis of H2S's known vasodilatory mechanisms.
- Postulation of H2S's role in cirrhosis pathogenesis.
Main Results:
- Hydrogen sulfide (H2S) is a novel gaseous transmitter.
- H2S induces vasodilation via K(ATP) channel activation in vascular smooth muscle cells.
- This mechanism aligns with observed vasodilation in cirrhosis.
Conclusions:
- H2S is implicated in regulating vascular tone.
- The vasodilatory effects of H2S may contribute to the hyperdynamic circulation in cirrhosis.
- Further research is warranted to confirm H2S's role in cirrhosis pathophysiology.