Portal Hypertension and Related Clinical Syndromes

The portal hypertension is initiated by the increased vascular resistance to portal blood flow and is primarily caused by structural changes such as fibrotic scar tissue and regenerative nodules compressing portal and central venules.Furthermore, previous reports showed that swelling of hepatocytes and capillarisation of hepatic sinusoids (loss of endothelial fenestrations and collagen deposition in the space of Disse) are part of the increased vascular resistance.The Increase in the portal vein blood flow occurs in a more advanced stage of portal hypertension and contributes to its maintenance and aggravation [1,2].Portal hypertension is usually caused by pre-hepatic abnormalities (e. g. portal or splenic vein thrombosis), post-hepatic abnormalities (e. g.Budd-Chiari syndrome) or intrahepatic non-cirrhotic causes (e. g. schistosomiasis, sinusoidal obstruction syndrome) however cirrhosis is by far the most common cause of portal hypertension and has been the most widely investigated [3].Portal hypertension is responsible for many of the manifestations of liver cirrhosis.Gastrointestinal bleeding as a result of ruptured gastroesophageal varices and from portal hypertensive gastropathy and colopathy, ascites and hepatorenal syndrome and hypersplenism are the direct consequences of portal hypertension itself.Other complications including spontaneous bacterial peritonitis, hepatic encephalopathy, cirrhotic cardiomyopathy, hepatopulmonary syndrome, and portopulmonary hypertension are also caused by pathophysiological pathway of portal hypertension [4]. Pathophysiology of Portal HypertensionPortal hypertension is primarily caused by the increase in both resistance to portal blood outflow and secondly by an increase in splanchnic blood flow and is associated with changes in the intrahepatic, systemic, and portosystemic collateral circulation.Alterations in vasodilatation and vasoconstriction play a central and pivotal role in the pathophysiology of portal hypertension by contributing to increased intrahepatic resistance, hyperdynamic circulation, and expansion of the collateral circulation [5]. Hepatic vasodilatorsNitric oxide: Nitric Oxide (NO), as a powerful endogenous vasodilator, modulates the intrahepatic vascular tone and is produced from the amino acid L-arginine by NO synthases.However, in the cirrhotic liver, NO synthesis is insufficient