These results demonstrate that low AT-III activity and further decreases in this activity are associated with PVT after splenectomy in cirrhotic patients, and that treatment with AT-III concentrates is likely to prevent the development of PVT in these patients.

With the technical standardization, LS becomes a feasible and safe approach in the setting of liver cirrhosis and portal hypertension.

In liver cirrhosis, down-regulation of endothelial nitric oxide synthase (eNOS) has been implicated as a cause of increased intrahepatic resistance. We investigated whether Rhokinase activation is one of the molecular mechanisms involved in defective eNOS signaling in secondary biliary cirrhosis. Liver cirrhosis was induced by bile duct ligation (BDL). We measured mean arterial pressure (MAP), portal venous pressure (PVP), and hepatic tissue blood flow (HTBF) during intravenous infusion of saline (control), 0.3, 1, or 2 mg/kg/hour fasudil for 60 minutes. In BDL rats, 1 and 2 mg/kg/hour fasudil significantly reduced PVP by 20% compared with controls but had no effect on HTBF. MAP was significantly reduced in response to 2 mg/kg/hour fasudil. In the livers of BDL rats, 1 and 2 mg/kg/hour fasudil significantly suppressed Rho-kinase activity and significantly increased eNOS phosphorylation, compared with controls. P ortal hypertension is a common clinical syndrome associated with liver cirrhosis and characterized by increased intrahepatic resistance and elevated splanchnic blood flow, leading to a pathological increase in portal pressure and the development of portosystemic collaterals such as esophagogastric varices. 1-6 Pharmacological therapy for portal hypertension should be aimed at reducing intrahepatic vascular tone or elevated splanchnic blood flow. However, the only available treatment is a nonselective beta-blocker that reduces portal venous pressure (PVP) by decreasing cardiac output and splanchnic blood flow. 7 Several randomized trials indicate that a nonselective beta-blocker is the first choice for primary and secondary prophylaxis against esophageal variceal bleeding. [8][9][10] However, the mean decrease in PVP in response to beta-blockers is only approximately 15%. Moreover, 15% of patients with cirrhosis are beta-blocker intolerant, whereas another approximately 30% do not respond to betablockers despite adequate blockade. 11 Therefore, there is a pressing need for a more effective pharmacological therapy for portal hypertension.Previous studies have shown that hepatic stellate cells (HSCs) through their contraction play a crucial role in regulating sinusoidal vascular tone. 12 The contractility of HSCs is regulated by the balance of vasoactive agents such as endothelin-1, and vasorelaxing agents such as nitric oxide (NO). 13 Recent studies have shown that the production of NO by endothelial nitric oxide synthase (eNOS) in hepatic sinusoidal endothelial cells (SECs) is Abbreviations: ␣-SMA, alpha-smooth muscle actin;

PHG may be associated with splenomegaly, and laparoscopic splenectomy may have a beneficial effect on PHG, at least for a short time.