Written informed consent to participate in the study was obtained from each patient. Inclusion criteria were age between 25 and 80 years and confirmed diagnosis of cirrhosis. Exclusion criteria were evidence of gastrointestinal
bleeding; portal vein thrombosis; diffuse or multinodular hepatocellular carcinoma not fulfilling Milano criteria; cardiac, renal or respiratory failure; previous surgical or intrahepatic portosystemic shunt; prescription of vasoactive drugs including beta-blockers and/or investigational drugs; bacterial infection or treatment with antibiotics in the preceding 2 weeks; or positive blood or ascitic fluid culture previous to hepatic hemodynamic study or presence of neutrocytic ascites (polymorphonuclear cell count >250 cells/mm3). Bacterial infection was ruled out by clinical history, physical examination, laboratory analysis, and both blood and ascitic fluid cultures performed in blood culture bottles.14 Other associated morbidities were excluded Selleck PD0325901 by clinical history, physical examination, electrocardiogram, and routine biochemical analysis. Per protocol, inclusion in the nonascites group was closed after 20 patients had been included. Patients were maintained on a sodium-restricted diet
and diuretics were withdrawn for 2 days before the hemodynamic study. No large-volume paracentesis was allowed in the preceding selleck kinase inhibitor 5 days. After fasting overnight, patients were transferred to the Hepatic Hemodynamic Laboratory. Under local anesthesia, 上海皓元医药股份有限公司 an 8-French venous catheter introducer (Axcess; Maxxim
Medical, Athens, TX) was placed in the right jugular vein under ultrasonographic guidance (SonoSite Inc, Bothell, WA) using the Seldinger technique. Under fluoroscopic control, a Swan-Ganz catheter (Edwards Laboratory, Los Angeles, CA) was advanced into the pulmonary artery for measurement of cardiopulmonary pressures and cardiac output (CO) by thermal dilution. A 7F balloon-tipped catheter (Medi-Tech; Boston Scientific Cork, Ltd., Cork, Ireland) was then advanced in to the main right hepatic vein to measure wedged and free hepatic venous pressures as previously described.2, 5, 15 All measurements were performed in triplicate in each study period, and permanent tracings were obtained on a multichannel recorder (Marquette Electronics, Milwaukee, WI). Portal pressure was estimated from the hepatic venous pressure gradient (HVPG), the difference between wedged and free hepatic venous pressure. The hepatic vascular resistance (dyne/second/cm−5) was estimated as: HVPG (mm Hg) × 80/hepatic blood flow (HBF) (L/minute).2, 5 Preceded by a priming dose of 5 mg, a solution of indocyanine green (Pulsion Medical Systems, Munich, Germany) was infused intravenously at a constant rate of 0.2 mL/minute. After an equilibration period of at least 40 minutes, four separate sets of simultaneous samples of peripheral and hepatic venous blood were obtained for the measurement of HBF as previously described.