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Disse’s space

A. Flow patterns in portal vein, Disse s space, and hepatocyte... [Pg.33]

Drugs exchange freely between blood and interstitium in the liver, where endothelial cells exhibit large fenestrations (100 nm in diameter) facing Disse s spaces (D) and where neither diaphragms nor basement membranes impede drug movement. [Pg.24]

Confirmation of the existence of perivascular lymphatic vessels by J. Disse ( Disse s space ), which had already been proposed by Th. MacGillavry in 1864. [Pg.13]

The liver forms more lymph than any other organ of the body (0.4-0.6 mg/kg BW/min). Lymph capillaries take up lymph from Disse s space (J. Disse, 1890) and thereafter from Mall s space (F.P. Mall, 1906), which lies between the limiting plate and the portal connective tissue. Disse s space is also considered to be the main source of lymph. In addition, lymph capillaries commence in the adventitia of sublobular veins and run close to the hepatic veins as far as the paracaval lymph nodes. Lymph vessels possess valves which permit the lymph to flow only in one direction. Lymphatic vessels are present in... [Pg.19]

Fig. 2.8 Spatial relationship of sinusoid and hepatic cells hepatocytes (H) in the form of boundary lamella (BL), cell nucleus (CN), canahculus (BC), Disse s space (D), endothelial cells (E), sieve plate (SP), Kuplfer cell (K), Ito cell (I). The cellular interchange area is increased by microvilli (modified from D. Sasse, 1986)... Fig. 2.8 Spatial relationship of sinusoid and hepatic cells hepatocytes (H) in the form of boundary lamella (BL), cell nucleus (CN), canahculus (BC), Disse s space (D), endothelial cells (E), sieve plate (SP), Kuplfer cell (K), Ito cell (I). The cellular interchange area is increased by microvilli (modified from D. Sasse, 1986)...
The stellate cells initially determined by K.W. von Kupffer (1876) by means of the gold chloride method were actually Ito cells located in Disse s space. It was not until 1898 and 1899 that the sinus macrophages were described by von Kupffer again - though at this point not sufficiently differentiated from the gold-reactive fatstoring cells. [Pg.21]

Ito cells (T. Ito, 1951) are also known as fat-storing cells, hepatic stellate cells or lipocytes. These long-lived cells, 5-10 im in size with long thin strands, lie in Disse s space (s. figs. 2.8, 2.9) and contain numerous cytoplasmic fat droplets as well as an abundance of vitamin A (= retinol ester). The retinol esters of the chylomicrons are absorbed by the hepatocytes and hydrolyzed into retinol. The latter is either passed to the blood by means of RBP or transported to Ito cells and stored. In the fat droplets of Ito cells, about 75% of the liver retinoids are present in the form of retinol esters. These fat droplets are characteristic of Ito cells they represent vacuolized... [Pg.21]

PIT cells were first demonstrated in the sinusoidal wall in rats (E. Witte et al., 1970). Later on, these lymphocytes with large granules and rod-cored vesicles were also found in the human liver, particularly in the sinusoids and in Disse s space. Due to their pseudopodia, they are variable. The proportion of PIT cells to Kupffer cells is 2 10. They are natural killer cells and destroy tumour cells or foreign cells as well as necrosed cells. It is not clear whether they have any additional endocrine function. Because of the strongly polarized distribution of their granulae, they could justifiably be classified as APUD cells. (6, 26, 27, 59, 68, 75)... [Pg.22]

Hepatocytes and sinusoidal cells are influenced by vegetative nerve fibre endings in Disse s space. [Pg.32]

An increase in blood both in the sinusoids and in Disse s spaces culminates in hepatomegaly. This can be witnessed particularly in cases of right heart failure, constrictive pericarditis, veno-occlusive disease and the Budd-Chiari syndrome. Inflammation-related hyper-aemia also occurs in acute viral hepatitis. [Pg.210]

The functions of the extracellular matrix are manifold (1.) stabilization of the tissue and organ structure, (2.) structural linkage of cells, (3.) transmission of information between the various types of cells within the tissue and the extracellular milieu, (4.) adhesion or migration of cells, and (5.) influence on the development and differentiation of cells and their polarity. In fibrogenesis, collagen fibres build the framework in which the other components of the extracellular matrix are embedded. In line with this wide scop>e of functions, the extracellular matrix is not only organ-sp>ecific as regards its architecture, but it also displays variations at different locations within the liver, e.g. in Disse s space, in the periportal fields and within the acinus zones. The extracellular matrix is a dynamic structure, i. e. there is a constant equilibrium between build-up (by matrix-metalloproteinases = MMP) and break-down (by tissue inhibitors of matrix metaUoproteinases = TIMP). [Pg.403]

Fibrosis is usually the consequence or concomitant symptom of a chronic hepatobiliary disease, the course of which can itself in turn be unfavourably influenced by the fibrosis. The matrix substances, which are being produced in greater quantities, are increasingly deposited in Disse s space in the portal field and periportal area as well as around the terminal liver vein. [Pg.405]

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)... [Pg.833]

The answer is 3 fCTiapter 8/7 B 2/. Cholestatic agents alter the ability of the bile canaliculi to transport bile salts. This activity may be related to osmotic changes caused by the secreted bile salts or to energy-dependent osmotic control accomplished through the sodium-potassium-adenosine triphosphatase (ATPase) pump. Cholestasis occurs in the bile canaliculi, and not in the common bile duct Kupffer cells, Disse s space, hepatic sinusoids, and the common bile duct are part of the hepatic parenchyma and are not directly involved in bile salt formation. [Pg.462]

Afterward, the microdroplets in nontumorous tissue flow via the sinusoid into the hepatic vein or Disse s space, which lies outside of sinusoidal space. The microdroplets entering Disse s space inevitably flow into the bile canalic-uli or lymphatic channels, finally out of the liver. In the HCC tissue the microdroplets remain there for a long time, probably because tumorous tissue is not equipped with a biliary or lymphatic drainage system. [Pg.268]

Figure 10.11 Diagram showing microarchitecture of vessels near HCC tissne. The hepatic artery branches off from feeding the tumor tissue to feeding other arteries as well as the sinusoid, the bile duct, and the portal vein. Blood flow through the tumor is drained more directly into the portal vein than into the sinusoids. A portion of serum in the sinusoids flows into Disse s space through which oil droplets is drained off as lymphatic flow. Figure 10.11 Diagram showing microarchitecture of vessels near HCC tissne. The hepatic artery branches off from feeding the tumor tissue to feeding other arteries as well as the sinusoid, the bile duct, and the portal vein. Blood flow through the tumor is drained more directly into the portal vein than into the sinusoids. A portion of serum in the sinusoids flows into Disse s space through which oil droplets is drained off as lymphatic flow.

See other pages where Disse’s space is mentioned: [Pg.154]    [Pg.24]    [Pg.32]    [Pg.20]    [Pg.21]    [Pg.22]    [Pg.24]    [Pg.247]    [Pg.406]    [Pg.526]    [Pg.763]    [Pg.812]    [Pg.556]    [Pg.451]   
See also in sourсe #XX -- [ Pg.24 , Pg.32 , Pg.33 ]

See also in sourсe #XX -- [ Pg.24 ]




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