| pubmed-article:18812641 | pubmed:abstractText | In last years significant progress in recognizing mechanisms of portal hypertension pathophysiology was done. However, some unclear topics in this disease still exist. Portal hypertension is primarily caused by the increase in resistance to portal outflow and secondly by an increase in splanchnic blood flow. Portal hypertension is associated with changes in the intrahepatic, systemic, and portosystemic collateral circulation. Alterations in vasoreactivity (vasodilation and vasoconstriction) play a central role in the pathophysiology of portal hypertension by contributing to increased intrahepatic resistance, hyperdynamic circulation, and expansion of the collateral circulation. Among vasoactive substances which are activated in portal hypertension nitric oxide (NO) is considered as the most important vasodilator. Endothelin-1 and cyclooxygenase-derived prostaglandins are the main vasoconstrictor factors. The imbalance between the hyperresponsiveness and overproduction of vasoconstrictors and the hyporesponsiveness and impaired production of vasodilators are the mechanisms responsible of the increased vascular one in the sinusoidal area of the liver. New concepts in the pathophysiology of portal hypertension find the significant role of hepatic stellate cells activated by endothelial factors which cause vascular remodeling as an adaptive response of the portal vessels wall. The most frequent causes of portal hypertension include portal vein thrombosis, storage diseases of the liver, hepatic cirrhosis (independent of etiology), hepatic veins thrombosis and schistosomiasis. Understanding the pathophysiology of portal hypertension could be of great utility in preventing and curing the complications of portal hypertension, such as esophageal varices, hepatic encephalopathy, ascites. | lld:pubmed |
