Hepatic veins

Liver and Gallbladder. High dosages of oral estrogens have been reported to increase the risk for jaundice, cholestatic hepatitis, gallstones, and hepatic vein blood clots. Estrogens promote the development of hepatic neoplasms associated with increased hepatic cell regenerative activity (186,187). 

Intoxicated patients surviving for 28 hours to 9 days had hepatocytes free in central or hepatic veins this finding was described as mobilization of liver cells. The role of methyl parathion in the induction of all of these lesions is unclear. 

Conjugated hyperbilirubinemia commonly results from blockage of the hepatic or common bile ducts, most often due to a gallstone or to cancer of the head of the pancreas. Because of the obstruction, bilirubin diglu-curonide cannot be excreted. It thus regurgitates into the hepatic veins and lymphatics, and conjugated bilirubin appears in the blood and urine (choluric jaundice). 

Iturriage, H., Ugarte, H. and Israel, Y, (1980). Hepatic vein oxygenation, liver blood flow and the rate of ethanol metabolism in recently abstinent alcoholic patients. Eur. J. Clin. Invest. 10, 211-218. 

The liver is a wedge-shaped organ of some 1.5 kg in adult humans, which, in terms of blood circulation, is interposed between the gastrointestinal tract and the rest of the body. The blood supply to the liver is from the hepatic portal vein (80%) and the hepatic artery (20%), the former bringing a rich supply of nutrients direct from the intestinal tract and the latter supplying the liver with oxygen. Blood drains from the liver by the hepatic vein. The position of the liver enables it to act as a processor of the absorbed nutrients, and to control their storage... 

Portal hypertension is a consequence of increased resistance to blood flow through the portal vein. Increased resistance is usually due to restructuring of intrahepatic tissue (sinusoidal damage) but may also be caused by presinusoidal damage such as portal vein occlusion from trauma, malignancy, or thrombosis. A third (and the least common) mechanism is outflow obstruction of the hepatic vein. This latter damage is posthepatic, and normal liver structure is maintained. This chapter will focus on portal hypertension caused by intrahepatic damage from cirrhosis. 

The liver is a large and distensible organ. As such, large quantities of blood may be stored in its blood vessels providing a blood reservoir function. Under normal physiological conditions, the hepatic veins and hepatic sinuses contain approximately 450 ml of blood, or almost 10% of blood volume. When needed, this blood may be mobilized to increase venous return and cardiac output. 

The ammonia produced from asparagine and glutamine is released into the hepatic portal vein, for removal by the liver and conversion to urea. The concentration of ammonia in the blood in the hepatic portal vein is about ten times higher than in the hepatic vein, indicating the quantitative importance of the liver in removing this ammonia. 

Classically the liver has been divided into hexagonal lobules centred around the terminal hepatic venules. Blood enters the liver through the portal tracts that are situated at the corners of the hexagon. The portal tracts are triads of a portal vein, an hepatic artery, and a common hepatic bile duct. The vast expanse of hepatic tissue, mostly consisting of parenchymal cells (PC) or hepatocytes, is serviced via terminal branches of the portal vein and hepatic artery, which enters the tissue at intervals. The hepatocytes are organized into cords of cells radially disposed about the central hepatic venule. Between these cords are vascular sinusoids that transport the blood to the central hepatic venules. The blood is collected through the hepatic venules into the hepatic vein which exits the liver into the inferior vena cava (Figure 4.1). 

Most drugs are absorbed from the small intestine before entering the hepatic vein on their way to the liver. Some drugs are substrates of efflux transporters, such as P-gp (e.g., diltiazem, estradiol see Table 5.1), which... 

The entry of a compound into the bloodstream does not necessarily ensure that it wiU arrive unchanged at its specific receptor. As mentioned before, xenobiotics absorbed from the gastrointestinal tract are carried by the portal vein to the liver. The liver has a very active xenobiotic-metabohzing system in which chemicals may or may not be altered before being released through hepatic veins into the general circulation. Alternatively, they may be excreted into the bile and returned to the gastrointestinal tract. From there they may be excreted, all or in part, or reabsorbed and carried back to the liver. 

Portal hypertension most commonly occurs as a consequence of chronic liver disease. Portal hypertension Is caused by Increased blood flow within the portal venous system and increased resistance to portal flow within the liver. Splanchnic blood flow is increased in patients with cirrhosis due to low arteriolar resistance that is mediated by increased circulating vasodilators and decreased vascular sensitivity to vasoconstrictors. Intrahepatic vascular resistance is increased in cirrhosis due to fixed fibrosis within the spaces of Disse and hepatic veins as well as reversible vasoconstriction of hepatic sinusoids and venules. Among the consequences of portal hypertension are ascites, hepatic encephalopathy, and the development of portosystemic collaterals—especially gastric or esophageal varices. Varices can rupture, leading to massive upper gastrointestinal bleeding. 

Two main blood vessels (Figure 15.1) enter the liver the hepatic artery carries oxygen-rich blood directly from the heart, while the hepatic portal vein carries blood from the spleen and nutrient-rich blood from the intestine. On leaving the liver, the blood is returned to the heart via the hepatic vein. 

Figure 6.3 Schematic representation of the arrangement and relationship of vessels and sinusoids in the liver. The central vein drains into the hepatic vein. Source Modified from Ref. 4.

Figure 21.3 Histochemical analysis of / -galactosidase gene expression in liver. Ten pa of pCMV-LacZ plasmid DNA were injected into a mouse via the tail vein using the hydrodynamics-based procedure, / -galactosidase gene expression was assayed eight hours post injection. HV, hepatic vein HA, hepatic artery PV, portal vein (50x). (see Color Plate 15)...

Young (<50 years) and no other cause found past history or family history of venous thrombosis, especially if unusual site (cerebral, mesenteric, hepatic veins) recurrent miscarriage thrombocytopenia cardiac valve vegetations livedo reticularis raised ESR malaise positive syphilis serology... 

Thrombophilia personal or family history of thrombosis (usually venous, particularly in unusual sites such as hepatic vein) at unusually young age... 

Blood is drained from the liver via three large hepatic veins, which ultimately drain into the IVC. 

The hepatic vessels may be visualised by conventional angiography or venography. These are invasive techniques requiring the injection of contrast media into the artery or vein via catheters during radiographic screening. Stenoses or occlusions are identified, e.g. occlusion of the hepatic veins in Budd-Chiari syndrome. 

The Budd-Chiari syndrome (BCS) is thought to be related to abnormal coagulation and is diagnosed by the identification of obstruction of large hepatic veins in the absence of tumour invasion or compression... 

Valla and colleagues [17], in a case-control study of 33 women with BCS, identified a relative risk of 2.37 for this complication in users of oral contraceptives, a figure very close to that for other vascular complications of the pill. Current evidence suggests that oral contraceptives lead to hepatic vein thrombosis by exacerbating an underlying throm-bogenic condition [16]. 

Valla D, Le MG, Paynard T, Rueff B, Benhamou JP (1986) Risk of hepatic vein thrombosis in relation to the recent use of oral contraceptives a case control study. Gastroenterology 90 967-972. 

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