Cirrhosis is a pathological entity characterized by the association of hepatocyte necrosis, fibrosis and regenerative nodules; hemodynamic and neurohormonal metabolic factors intervening in its development mechanisms, resulting in hepatic stellate cell activation and transformation and development of liver fibrosis.

Cytokines are key modulators of liver cell fibroblast transformation. Prostaglandins play an important role in the control of vascular tone and in thrombosis; Angiotensin II stimulates fibroblast proliferation by AT-1 receptors. Thrombin influences cellular remodeling in the liver and cardiovascular cirrhotic patients. Oxidative stress is involved in the development of liver cirrhosis by primary and secondary biological irreversible effects. Complex etiology involving vasoactive substances, oxidative stress in the pathogenesis of liver cirrhosis, require further studies to elucidate the mechanisms involved in hemodynamic disturbances associated with this disorder.