Circulating endogenous cannabinoid anandamide and portal, systemic and renal hemodynamics in cirrhosis
Version of Record online: 9 AUG 2004
Volume 24, Issue 5, pages 477–483, October 2004
How to Cite
Fernández-Rodriguez, C. M., Romero, J., Petros, T. J., Bradshaw, H., Gasalla, J. M., Luisa Gutiérrez, M., Lledó, J. L., Santander, C., Pérez Fernández, T., Tomás, E., Cacho, G. and Michael Walker, J. (2004), Circulating endogenous cannabinoid anandamide and portal, systemic and renal hemodynamics in cirrhosis. Liver International, 24: 477–483. doi: 10.1111/j.1478-3231.2004.0945.x
- Issue online: 12 OCT 2004
- Version of Record online: 9 AUG 2004
- Received 28 August 2003, accepted 3 May 2004
- hemodynamic disturbance of cirrhosis
Abstract: Background: Endocannabinoids may participate in the homeostasis of arterial pressure. Recently, anandamide, the most extensively studied endocannabinoid, has been proposed as a key mediator in the peripheral arterial vasodilation of cirrhosis.
Objectives: To determine if circulating levels of anandamide are related to the extent of the peripheral arterial vasodilation, the severity of portal hypertension and the degree of liver and renal dysfunction of patients with cirrhosis.
Methods: Plasma levels of anandamide and several systemic, portal and renal hemodynamic parameters were determined in 18 patients with cirrhosis and eight healthy subjects (control group).
Results: Plasma levels of anandamide were elevated in patients compared to the control group (P<0.05), nevertheless, no differences between patients with ascites and well-compensated patients were found. There was no correlation between anandamide concentration and arterial pressure, cardiac output and systemic vascular resistance, Child–Pugh's score, portal pressure, renal vascular resistance, plasma renin activity or plasma aldosterone concentration.
Conclusions: Circulating levels of anandamide are increased in cirrhotic patients. However, this elevation was unrelated to the extent of arterial vasodilation, the severity of portal hypertension or the degree of hepatic and renal dysfunction. Although a local hormonal action cannot be excluded, our results do not support a relevant contribution of this system in the hemodynamic disturbance of cirrhosis.