Prehepatic portal hypertension and mitochondrial dysfunction in brain hippocampus

PERAZZO, J.C.; LORES ARNAIZ, S.; FERNÁNDEZ, M.A.; LAGO, N.; LEMBERG, A.

Hepatic Encephalopathy and Nitrogen Metabolism

Springer

Lugar: Berlin; Año: 2006; p. 194 - 201

Introduction. During its progressive evolution chronic liver disease develops to a systemic pathology. Almost all organs participate and serious complications can appear in liver itself or in distant tissues, such as the lung, oesophagus or central nervous system (CNS).  Portal Hypertension (PH) is mainly the result of obstruction to the hepatic blood flow, may be clinically silent and is often discovered due to late complications. PH can be classified according to the organ or vessel that contains the obstructing lesion (1). Another classification is based on measurements of hepatic venous pressure and distinguishes between presinusoidal, sinusoidal and post-sinusoidal PH (2,3).  Hepatic encephalopathy (HE) constitutes one of the most intriguing complications in acute and chronic liver pathology. In addition to clinically manifest HE, a subclinical stage has been described (4). Beside this, the final report of the working party at the 11th World Congress of Gastroenterology (5) defined HE into three Types (A, B and C) and Type B was defined as: "HE associated with portal-systemic bypass with no intrinsic hepatocellular disease". Experimental prehepatic portal hypertension induced by portal vein ligation (PPH) could be regarded as valid model for the study of prehepatic portal hypertension and it also could be considered as a subclinical or a low-grade model of HE. Moreover, PPH rats display several functional and ultrastructural changes in the CNS. Among these it is important to point out the mitochondrial morpho-functional changes in blood-brain barrier (BBB).