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Related Experiment Video

Updated: Jul 12, 2026

Visualization and Analysis of Blood Flow and Oxygen Consumption in Hepatic Microcirculation: Application to an Acute Hepatitis Model

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Hyperdynamic circulation in cirrhosis: a role for nitric oxide?

P Vallance¹, S Moncada

¹Wellcome Research Laboratories, Langley Court, Beckenham, Kent, UK.

Lancet (London, England)

|March 30, 1991

Summary

Cirrhosis causes hypotension due to increased nitric oxide (NO) production. This potent vasodilator, nitric oxide, leads to low vascular resistance and reduced sensitivity to vasoconstrictors in patients with liver disease.

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Published on: February 24, 2018

Area of Science:

Cardiovascular Physiology
Hepatology
Vascular Biology

Background:

Cirrhosis is characterized by hypotension, low systemic vascular resistance, and diminished vasoconstrictor sensitivity.
These hemodynamic alterations may stem from an overproduction of vasodilators.
Nitric oxide (NO) is a key vasodilator synthesized and released by peripheral blood vessels.

Purpose of the Study:

To investigate the role of nitric oxide (NO) in the cardiovascular changes associated with cirrhosis.
To explore the potential link between endotoxemia in cirrhosis and sustained NO synthase induction.

Main Methods:

Review of existing animal studies on endotoxin and cytokine-induced NO synthase expression.
Analysis of the physiological effects of sustained NO release on vascular tone.
Correlation of endotoxemia prevalence in cirrhosis with observed hemodynamic changes.

Main Results:

Animal studies demonstrate that bacterial endotoxin and cytokines induce NO synthase, leading to sustained NO release and hypotension.
Endotoxemia is a frequent complication in patients with cirrhosis.
Persistent induction of NO synthase is hypothesized to underlie the characteristic hemodynamic profile of cirrhosis.

Conclusions:

Increased synthesis and release of nitric oxide (NO) likely contribute significantly to the hypotension and low systemic vascular resistance seen in cirrhosis.
The persistent induction of NO synthase, potentially triggered by endotoxemia common in cirrhosis, may explain these sustained hemodynamic changes.
Targeting NO production pathways could offer therapeutic strategies for managing cardiovascular dysfunction in liver disease.