Circulating nitric oxide products do not solely reflect nitric oxide release in cirrhosis and portal hypertension
Article first published online: 5 JUL 2011
© 2011 John Wiley & Sons A/S
Volume 31, Issue 9, pages 1381–1387, October 2011
How to Cite
Afzelius, P., Bazeghi, N., Bie, P., Bendtsen, F., Vestbo, J. and Møller, S. (2011), Circulating nitric oxide products do not solely reflect nitric oxide release in cirrhosis and portal hypertension. Liver International, 31: 1381–1387. doi: 10.1111/j.1478-3231.2011.02576.x
- Issue published online: 6 SEP 2011
- Article first published online: 5 JUL 2011
- Received 28 February 2011, Accepted 6 June 2011
- hyperdynamic circulation;
- pulmonary function;
- renin-angiotensin-aldosterone system
Background: Patients with cirrhosis often develop a systemic vasodilatation and a hyperdynamic circulation with activation of vasoconstrictor systems such as the renin–angiotensin–aldosterone system (RAAS), and vasopressin. Increased nitric oxide (NO) synthesis has been implicated in the development of this state of vasodilation and pulmonary dysfunction including increased exhaled NO concentrations. Circulating metabolites (NOx) may affect the systemic and pulmonary NO-generation. However, the relations of these abnormalities to the haemodynamic changes remain unclear.
Aims: The aims of the present study were to measure changes in exhaled NO in relation to circulating NOx, RAAS, and haemodynamics.
Methods: Twenty patients (eight child class A and 12 class B patients) underwent a liver vein catheterization with determination of splanchnic and systemic haemodynamics. Circulating NOx and exhaled NO were determined in the supine and sitting positions and related to haemodynamics, RAAS and lung diffusing capacity (DLCO). Eight matched healthy individuals served as controls.
Results: All patients with cirrhosis had portal hypertension. We found no significant difference in exhaled NO between patients and controls and no changes from the supine to the sitting position. Exhaled NO in the patients correlated significantly with plasma volume, heart rate and DLCO. NOx concentrations were not significantly increased in the patients. NOx correlated with portal pressure and haemodynamic indicators of vasodilatation, but not with exhaled NO concentrations.
Conclusion: In patients with moderate cirrhosis, exhaled NO is normal. Circulating NOx do not seem to reflect pulmonary and systemic NO release, but NOx seems to reflect systemic and splanchnic haemodynamic changes in cirrhosis.