Hemodynamics in the isolated cirrhotic liver

Abstract

Increased intrahepatic resistance is the initial event to the increased portal pressure and development portal hypertension in cirrhosis. Narrowing of the sinusoids due to anatomic changes is the main component of the increased intrahepatic resistance. However, a dynamic component is also involved in the increased vascular tone in cirrhosis. The imbalance between the hyperresponsiveness and overproduction of vasoconstrictors (mainly endothelin-1 and cyclooxygenase-derived prostaglandins) and the hyporesponsiveness and impaired production of vasodilators [mainly nitric oxide (NO)] are the mechanisms responsible of the increased vascular tone in the sinusoidal/postsinusoidal area. In contrast, the vascular resistance in the hepatic artery, which is determined in the presinusoidal area, is decreased due to increased vasodilators (NO and adenosine). This suggests different availabilities of NO in the intrahepatic circulation with preserved production in the presinusoidal area and impaired production in the sinusoidal/postsinusoidal area.