Central hepatic vein

Fig. 1.18 Illustration of liver lobules and vessels by F. KmRNAN, 1833 (a, b interlobular veins, c intralobular vein plexus, d intralobular branch of the central hepatic vein) (13)...

The perivascular fibrous capsule (R Glisson, 1654) commences in the hepatic porta as a tree-like branching framework of connective tissue surrounding the interlobular vessels. It also surrounds the central hepatic vein and its small tributaries, which are joined to the parenchyma by radial fibres as well as being established in the portal tracts. This prevents a suction-induced collapse of the venous vessels as a result of respiration-dependent negative pressure in the pleural cavity. The perivascular connective tissue, known as Glisson s capsule, extends fine secondary trabeculae into the parenchyma. They contain the intralobular biliary, lymphatic and blood capillaries. 

Fig. 2.7 Reticular fibre nefwork with central hepatic vein (CHV) (Gomori s reticulin stain)...

Fig. 2.15 Diagram of the liver lobule and the acinus arranged like a clover leaf around the portal field according to the acinar structure (modified from D. Sasse, t986) central hepatic vein (CV) or terminal hepatic vein, periportal field (P). Circulatory and meta-bolically different zones zone t (periportal), zone 2 (intermediate), zone 3 (perivenous)...

The oral route of exposure in dogs to high concentrations leads to vomiting, diarrhea, and death. The major histopathological findings were centrilobular hepatic necrosis. The necrosis included the central hepatic veins and their respective tributaries. Bromobenzene was not found to be mutagenic in the Ames assay. 

Macroscopically, EHE presents as multiple nodules or large intrahepatic mass, the latter being the natural evolution of multiple confluent nodules (Miller et al. 1992). EHE characteristically has a fibrotic hypo-vascular central area and a peripheral hyperemic rim. At the outer edge of these tumors there is often a narrow avascular zone where hepatic sinusoids and small vessels are infiltrated by advancing tumor (Miller et al. 1992). The hepatic capsule overlying an EHE is frequently retracted inward, probably due to fibrosis induced by the tumor. The neoplastic tissue is composed of epithelioid cells that proliferate into the sinusoids and central hepatic veins. 

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. 

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). 

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.

In the Budd-Chiari syndrome, the central area of the liver shows a normal or even increased concentration of radioactivity, whereas the peripheral regions of both lobes of liver exhibit reduced or even no uptake ( hot spots and multiple focal storage defects). Only the caudate lobe shows increased activity due to its separate venous flow, it is not functionally affected by hepatic vein thrombosis. (26)... 

The most frequent cause of posthepatic portal hypertension is right ventricular insufficiency. The central venous pressure is transferred to the hepatic veins and the sinusoids. Constrictive pericarditis leads to a state of pronounced posthepatic portal hypertension with the early development of ascites. Severe tricuspid valve incompetence also culminates in this condition. A membranous obstruction of the inferior vena cava was likewise described in 1968 as a genetically determined cause of posthepatic portal hypertension (S. Yamamoto et al.). Three variants can be distinguished by angiography, depending on the different ways in which the hepatic veins are involved or whether they are affected at all. Thrombosis of the inferior vena cava can develop either from thrombosis of the pelvic veins or independently in the presence of predisposing factors. 

I.) The hepatic flow volume is 20-25% of the CO and is thus directly dependent on the cardiac ejection volume. (2.) The pressure in the lesser circulation is transferred directly to the valveless hepatic veins and may thus also reach the central veins. 

The Budd-Chiari syndrome (BCS) is defined as partial or complete obstruction of the hepatic veins due to thrombosis. This may affect the whole hepatic venous system from the central vein to the large hepatic veins, even as far as the opening of the inferior vena cava into the right atrium. However, the obstruction can simply occur in individual branches of the hepatic veins and thus affect only certain areas of the liver. The syndrome may have an acute onset or begin insidiously and take a chronic course. The clinical picture is usually characterized by the Chiari triad hepatomegaly, abdominal pain and ascites. 

Veno-occlusive disease (VOD) is characterized by thrombosis of the central and small (sublobular) hepatic veins. It is also known as the radicular form of the Budd-Chiari syndrome or as the Stuart-Bras syndrome, (s. tab. 14.5) (75, 92, 93)... 

Histology provides useful diagnostic evidence. Sinusoidal endothelial damage can be found, including extra-vascular accumulation of erythrocytes in Disse s spaces as well as subendothelial oedema and cellulation. After 2 to 3 days, delicate fibres appear within the central and sublobular veins, occasionally also in the medium-sized hepatic veins, ultimately resulting in occlusion of the lumen. Fibrotic thickening of the vessel walls occurs. Stenosis and thrombosis of the small hepatic veins cause extensive sinusoidal congestion. The liver cells become necrotic or atrophic. Micronodular cirrhosis develops in a chronic course, (s. fig. 29.10)... 

Devin F, Roques G, Disdier P, Rodor F, Weiller PJ. Occlusion of central retinal vein after hepatitis B vaccination. Lancet 1996 347(9015) 1626. 

The functional anatomical unit of the hver is the acinus, adjacent to the portal triad, which consists of a branch of the portal vein, hepatic artery, and bile duct. Each acinus is a diamond-shaped mass of liver parenchyma that is supplied by a terminal branch of the portal vein and of the hepatic artery and drained by a terminal branch of the bile duct. The blood vessels radiate toward the periphery, forming sinusoids, which perfuse the liver and ultimately drain into the central (terminal) hepatic vein (Figure 47-2). The sinusoids... 

To understand the possibilities and limitations of liver in vitro systems it is crucial to be aware of the organization principles of this organ. The smallest functional unit of the liver is the lobule (Fig. la). The human liver is composed of approximately one million lobules. Each lobule is supplied by branches of the portal vein which carries blood from the intestine (about 80 % of the liver s blood). Moreover, arterial blood is supplied by branches of the liver artery (about 20 %). The blood enters the lobules in the periphery, passes through microvessels where it is in close contact with hepatocytes, is finally drained off into the central veins, and leaves the liver by the hepatic vein. The oxygen concentration is about 13 % v/v (60-65 mmHg) in the periportal zone and drops to about 4 % v/v (30-35 mmHg) in the central vein [3]. 

Arterial and venous blood from the portal triad passes through the hepatic lobules to the central veins via the hepatic sinusoids. After passing through the hepatic lobules, blood collects in the central veins, which ultimately coalesce into the hepatic veins, which then enter the inferior vena cava. 

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. From Timbrell, J.A., The liver as a target organ for toxicity, in Target Organ Toxicity, edited G.M.Cohen (Boca Raton, FI CRCPress), 1989, with permission. 

The precise pathogenesis of the central nervous system (CNS) signs and symptoms that accompany liver failure (hepatic encephalopathy) in patients such as Percy Veere is not completely understood. These changes are, however, attributable in part to toxic materials that are derived from the metabolism of nitrogenous substrates by bacteria in the gut that circulate to the liver in the portal vein. These materials "bypass" their normal metabolism by the liver cells, however, because the acute inflammatory process of viral hepatitis severely limits the ability of liver cells to degrade these compounds to harmless metabolites. As a result, these toxins are "shunted" into the hepatic veins unaltered and eventually reach the brain through the systemic circulation ("portal-systemic encephalopathy"). 

Macroscopically, a mass that involves both the right and left lobes will be found in 70% of cases. On histological analysis HCC will show giant tumor cells with large trabeculae arranged in an acinar pattern. Necrosis and vascular involvement are commonly seen. Often there is vascular invasion of the portal system and less frequently that of the hepatic vein and IVC. A variant of HCC is fibrola-mellar HCC, which will present with a central scar in 76% of patients on macroscopic examination. 

The diverse metabolic activities of the liver make it susceptible to solvent induced in-jiuy, particularly from reactive intermediates which damage cellular macromolecules. The microscopic anatomy of the liver provides an explanation for this susceptibility. The basic unit of the liver is the hepatic lobule which consists of a central vein surrounded radially by sinusoids of liver cells (hepatocytes). Portal triads consisting of a hepatic artery, a hepatic vein and a bile canniliculus are located at the periphery. Liver cells closest to the vascular... 

The acinus is that portion of liver supplied by a primary afferent branch of the portal vein and hepatic artery. If we look at a bell-shaped hepatic lobule hanging from and traversed by a branch of the hepatic vein, the portal space runs on its side containing the artery, the vein, and the bile duct (see Figs. 9-21 and 9-22). At some point the vein and the arteriole yield three branches, two lateral and one apical, that are the primary afferent branches. They leave the connective tissue of the portal tract to penetrate in the substance of the lobule, where they further ramify into smaller branches that enter the sinusoid of the lobule. The territory irrigated by these primary afferent arterioles, the acinus, forms a somewhat irregular ovoid mass of tissue inserted between two central veins. The tissue mass is composed mainly of hepatic cells and sinusoids lined by Kupffer s cells. The central zone of the acinus (zone 1) receives the fresh blood supply and may therefore be the first to be injured by toxins in blood. The peripheral zone (zone 3) receives a blood supply partially exhausted in its oxygen and nutrients and is therefore more susceptible to anoxemia. 

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