Disease relevance of Hepatic Veins

• Although membranous obstruction of the inferior vena cava is frequently assumed to be a congenital defect, it has recently been hypothesized that it could be acquired and secondary to thrombosis at the ostium of hepatic veins [1].
• These findings demonstrate that absent or reversed flow in the hepatic veins and/or flat flow in the hepatic veins associated with reversed flow in the inferior vena cava may be considered diagnostic for the Budd-Chiari syndrome [2].
• Although obstruction of the inferior vena cava caused by rupture of an abdominal aortic aneurysm is known to occur, obstruction without rupture and involving the hepatic veins has not been previously reported [3].
• A 24-yr-old woman with hemolytic anemia developed multiple thrombosis of the hepatic vein and inferior vena cava [4].
• In patients with short-length hepatic vein stenosis, splenomegaly (28% vs. 55%, P < .05) and hypersplenism were significantly less common; serum transaminase (P < .001) and creatinine levels (P < .02) were lower, prothrombin was higher (P < .001), and 5-year survival was significantly better (Kaplan-Meier estimates: 80% vs. 50%, P < .05) [5].

High impact information on Hepatic Veins

• After 3 hours, the specific activity of uridine in the hepatic vein was more than three times that in the arterial circulation [6].
• Therefore, we investigated SGU in six patients with NIDDM and six weight-matched control subjects by means of the hepatic vein catheterization (HVC) technique [7].
• We validated this method in 12 nondiabetic subjects using hepatic vein catheterization (HVC) during an oral glucose tolerance test [8].
• L-(1-13C,15N)leucine, L-(ring-2H5)phenylalanine, and L-(ring-2H2) tyrosine were infused intravenously, and isotopic enrichments of [1-13C,15N]-leucine, (13C)leucine, (13C)ketoisocaproate, (2H5)phenylalanine, [2H4]tyrosine, (2H2)tyrosine, and 13CO2 were measured in arterial, hepatic vein, and femoral vein samples [9].
• When the perfusate contained 200 mM thiourea, the comparable recovery of [14C]urea from the hepatic veins exceeded that of 3HOH by a factor of 3.48 +/- 0.44 (n = 7) [10].

Chemical compound and disease context of Hepatic Veins

• We studied 14 patients with portal hypertension and cirrhosis using portal and hepatic vein catheterizations to determine the effects of transdermal application of nitroglycerin tape (containing 10 mg of nitroglycerin and capable of releasing 6 to 7 mg of nitroglycerin in 12 hr) on splanchnic hemodynamics [11].
• Collagenisation also correlated with CCLI (P less than 0.001), serum bilirubin (P less than 0.001), serum aspartate transferase (SGOT) (P less than 0.003), and clinical evidence of portal hypertension and histological changes of necrosis, inflammation, and terminal hepatic vein sclerosis [12].
• In basal conditions and after an intravenous ethanol infusion (1 g/kg body weight), hepatic venous pressure gradient and hepatic blood flow using indocyanine green were measured through hepatic vein catheterization [13].
• The effects of somatostatin and vasopressin on blood gases, pulmonary and systemic hemodynamics, and portal pressure assessed by the gradient between occluded and free hepatic vein pressures, were investigated in 18 patients with liver cirrhosis [14].
• AIMS: To study the serum and hepatic vein concentration of ET-1, ET-2, ET-3 and nitric oxide in patients with primary biliary cirrhosis and the effect of ursodeoxycholic acid treatment [15].

Biological context of Hepatic Veins

• No correlation could be demonstrated between hepatic venous pressure gradient and the concentration of prostanoids in the hepatic vein with the exception of thromboxane B2 (r = 0.55, p less than 0.05) [16].
• Assessment in the cirrhotics included measurement of hepatic vein pressure gradient, indocyanine green extraction ratio, indocyanine green clearance, and antipyrine clearance as indices of portal pressure, intrahepatic shunting, hepatic blood flow and functional hepatocellular mass, respectively [17].
• Ethanol did not produce a significant change in wedged hepatic-vein pressure, free hepatic-vein pressure, azygous blood flow, mean arterial pressure or heart rate compared with the effects of 5% dextrose in water alone [18].
• The effect of intraperitoneal pressure was then studied by measuring glomerular filtration rate, renal plasma flow, pressure in the vena cava, hepatic vein free flow, and hepatic vein wedged pressure before, during, and after paracentesis to reduce the intraperitoneal pressure from 30 to 40 cm H2O to 12 to 17 cm H2O [19].
• Hepatic blood flow, cardiac output and the oxygen contents were measured in the radial and pulmonary arteries and in the hepatic veins before and 45 min after intravenous administration of clonidine, 150 micrograms [20].

Anatomical context of Hepatic Veins

• The concentration of uridine in the hepatic vein of the rat was essentially the same as that in the arterial circulation and portal vein [6].
• To determine the metabolism of 3,3'-T2 and 3',5'-T2 in human liver and kidneys plasma samples were obtained from (a) a brachial artery and a hepatic vein in 20 normal subjects, and from (b) a femoral artery and a renal vein in 11 normal subjects [21].
• All patients with interrupted inferior vena cava, azygous continuation to the superior vena cava, and hepatic veins draining to the right atrium (polysplenia syndrome) were reviewed to determine the incidence of PAVMs in those with CVPA (ie, hepatic venous flow excluded from the pulmonary arteries) and without CVPA [22].
• Evidence that interaction of hepatocytes with the collecting (hepatic) veins triggers position-specific transcription of the glutamine synthetase and ornithine aminotransferase genes in the mouse liver [23].
• Injections of vasopressin into the inferior vena cava at the level of the hepatic veins consistently produced smaller hepatic vascular effects than either intra-arterial or intraportal injections of the same doses [24].

Associations of Hepatic Veins with chemical compounds

• Splanchnic exchange of glucose and gluconeogenic precursors was measured using the hepatic vein catheter technique [25].
• Evidence that supports that assumption was obtained by comparing the randomization of 14C in the urinary glucuronide with that in glucose in blood from the hepatic vein of four of the subjects before and after they were given glucagon [26].
• MAIN OUTCOME MEASURES: Radiotracer-derived measures of norepinephrine release to plasma, central hemodynamics, wedge hepatic vein pressure, and measures of renal function [27].
• The HVI-CHP system was used to determine directly the doxorubicin plasma concentration in the hepatic vein and the hepatic venous flow rate, and simultaneously, to eliminate hepatic re-entry of the drug [28].
• Propranolol has been reported to reduce portal and wedged hepatic vein pressures in man and may be useful for the prevention of variceal bleeding [29].

Gene context of Hepatic Veins

• METHODS: Peripheral vein (and hepatic vein in patients undergoing transjugular liver biopsy) chemokine concentrations were measured by ELISA [30].
• There was a significant correlation in the hepatic vein between fasting IGF-I and IGFBP-3 levels (r = 0.928; P < 0.001) [31].
• The levels of MIP-2 and CINC in the hepatic vein, and tumor necrosis factor (TNF)-alpha, which stimulates these chemokine production, were also monitored [32].
• Expressions of adhesion molecules in vessels were not enhanced except ELAM-1 of the hepatic vein [33].
• The level of interleukin-8 and interleukin-1 receptor antagonist was significantly higher in the hepatic vein than in the artery (P < 0.05) [34].

Analytical, diagnostic and therapeutic context of Hepatic Veins

• Evaluation by arteriography, venography, and computed tomography revealed compression and venous obstruction at the confluence of the hepatic veins and inferior vena cava [3].
• Flow velocities in the superior vena cava and hepatic vein were also obtained by pulsed-wave Doppler echocardiography from the supraclavicular and subcostal views, respectively [35].
• A patient with the Budd-Chiari syndrome due to membranous obstruction of the right hepatic vein and long segmental obstruction of the inferior vena cava who was successfully treated with percutaneous transluminal angioplasty is described [36].
• METHODS: After the cranial dissection of the suprahepatic inferior vena cava (IVC) between the middle and left hepatic veins, a long light curved Kelly clamp is inserted from the caudal edge behind the caudate lobe and passed cranially along the anterior midline of the IVC [37].
• Review of the literature revealed 14 prior cases of balloon dilatation of the hepatic venous system: 10 of the hepatic portion of the inferior vena cava, three of the right hepatic vein, and one of the left hepatic vein [36].

References