Hemodynamic and antifibrotic effects of a selective liver nitric oxide donor V-PYRRO/NO in bile duct ligated rats.

Aim: To assess whether a liver specific nitric oxide (NO) donor (V-PYRRO/NO) would prevent the development of portal hypertension and liver fibrosis in rats with bile duct ligation (BDL).

Methods: Treatment (placebo or V-PYRRO/NO 0.53 micromol/kg per hour) was administered i.

Terlipressin inhibits in vivo aortic iNOS expression induced by lipopolysaccharide in rats with biliary cirrhosis.

In cirrhosis, lipopolysaccharide (LPS, a product of Gram-negative bacteria) in the blood may cause septic shock. LPS-elicited induction of arterial inducible nitric oxide synthase (iNOS) results in nitric oxide (NO)-induced vasodilation, which causes arterial hypotension and hyporeactivity to alpha(1)-adrenergic constrictors. In vitro studies have suggested that vasopressin inhibits iNOS expression in cultured vascular smooth muscle cells exposed to LPS.

Evolution of hypoxemia in patients with severe cirrhosis.

Background And Aim: Hypoxemia is common in patients with cirrhosis but the natural history of this syndrome is unknown. The aim of this study was to follow a series of patients with cirrhosis and to compare patients with and without hypoxemia to determine their risk of complications and survival rate.

Methods: Fifty-eight consecutive Child-Pugh C patients with cirrhosis were included and followed up for 1-18 months.

Clinical course, predictive factors and prognosis in patients with cirrhosis and type 1 hepatorenal syndrome treated with Terlipressin: a retrospective analysis.

Background And Aim: Terlipressin has been proposed to treat renal failure in patients with type 1 hepatorenal syndrome (HRS). However, the predictive factors for improved renal function and survival are unknown in patients with type 1 HRS treated with terlipressin. The aim of the present retrospective study was to investigate the predictive factors and prognosis of patients with type 1 HRS treated with terlipressin.

Role of shear stress in aortic eNOS up-regulation in rats with biliary cirrhosis.

Background & Aims: In rats with portal vein stenosis, the initial cause of aortic nitric oxide (NO) overproduction might be overactivation of endothelial NO synthase (eNOS) related to increased shear stress. Cardiac output is higher in cirrhosis than in extrahepatic portal hypertension. The aims of this study were to evaluate the role of shear stress, vascular endothelial growth factor (VEGF), and cytokines in aortic eNOS up-regulation in rats with biliary cirrhosis and to compare these results with those in rats with portal vein stenosis.

Relationship between protein kinase C alterations and nitric oxide overproduction in cirrhotic rat aortas.

Background: Although nitric oxide (NO) overproduction and protein kinase C (PKC) alterations may play a role in systemic haemodynamic changes in cirrhotic rat aortas, the relationship between NO synthase (NOS) hyperactivation and PKC hypoactivation is unknown. Therefore, the relationships between NOS and PKC activities were studied in cirrhotic rat aortas.

Methods: The effects of NOS inhibition by Nw-nitro-L-arginine (LNNA) on the contractile response to phorbol myristate acetate (PMA), a PKC activator, were studied.

Pulmonary hemodynamics and gas exchange after liver transplantation in patients with cirrhosis.

In patients with cirrhosis, discrepant findings have been reported on the evolution of pulmonary hemodynamics and gas exchange after liver transplantation. The aim of this study was to evaluate the effects of liver transplantation on pulmonary and systemic hemodynamics and gas exchange in patients transplanted for cirrhosis. Forty-three patients with cirrhosis underwent hemodynamic investigations before and one year after liver transplantation.