Liver sinusoids

McCuskey, R.S. Morphological mechanisms for regulating blood flow through hepatic sinusoids. Liver 2000 20 3—7... 

Groot PHE, Van Berkel TJC, Van Tol A (1981) Relative contributions of parenchymal and non-parenchymal (sinusoidal) liver cells in the uptake of chylomicron remnants. Metabolism 30 792-797... 

Figure 16. Schematic of the geometry of a section of liver before (top) and after (bottom) being subjected to slow freezing. During slow freezing, ice forms in the sinusoids and water flows osmotically from the cells into the sinusoids. (The upper drawing is slightly modified from Rubinsky and Pegg, 1988.)...

M (increased absolute and relative liver weight dilation of sinusoids necrosis)... 

Goresky CA. A linear method for determining liver sinusoidal and extravascular volumes. Am J Physiol 1963 204 626-40. 

In the liver, the bilirubin is removed from albumin and taken up at the sinusoidal surface of the hepato-cytes by a carrier-mediated saturable system. This facilitated transport system has a very large capacity, so that even under pathologic conditions the system does not appear to be rate-limiting in the metabolism of bilirubin. 

Unlike the liver injury that occurs with toxic chemicals (see above), reperfusion injury affects not only the hepatocytes but also the endothelial cells that line the sinusoids as an important primary target. It is thought that there may be some aspects of preservation-reperfusion injury that are unique to the liver and UW solution is apparently more effective in this tissue than in others (Clavien aal., 1992). The principle characteristic of this injury is that it involves damage to the sinusoidal cells such that leucocytes and platelets are stimulated to adhere on reperfusion. 

Under normal conditions the sinusoidal endothelial cells are flat thin cells lying close against the hepatocyte surface, separated only by the periplasmic space. Cold preservation of the liver causes the endothelial cells to round up and detach, although they are not actually... 

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. 

Sinusoidal damage from cirrhosis is the most common cause of portal hypertension. The sinusoids are porous vessels within the liver that surround radiating rows of hepatocytes, the basic functional cells of the liver (Fig. 19-2). Progressive destruction of hepatocytes and an increase in fibroblasts and connective tissue surrounding the hepatocytes culminate in cirrhosis. Fibrosis and regenerative nodules of scar tissue... 

The sinusoids transport both portal and arterial blood to the hepatocytes. The systemic blood delivered to the liver contains nutrients, drugs, and ingested toxins. The liver processes the nutrients (carbohydrates, proteins, lipids, vitamins, and minerals) for either immediate use or for storage, while the drugs and toxins are metabolized through a variety of processes known as first-pass metabolism. The liver also processes metabolic waste products for excretion. In cirrhosis, bilirubin (from the enzymatic breakdown of heme) can accumulate this causes jaundice (yellowing of the skin), scleral icterus (yellowing of the sclera), and tea-colored urine (urinary bilirubin excretion). 

Meier, P. J., et al. Substrate specificity of sinusoidal bile acid and organic anion uptake systems in rat and human liver. Hepatology 1997, 26, 1667-1677. 

Zimmerli, B., J. Vaiantinas, and P. J. Meier. Multispecificity of Na+-dependent taurocholate uptake in basolateral (sinusoidal) rat liver plasma membrane vesicles. J. Pharmacol. Exp. Ther. 1989, 250, 301-318. 

The liver plays an important role in determining the oral bioavailability of drags. Drag molecules absorbed into the portal vein are taken up by hepatocytes, and then metabolized and/or excreted into the bile. For hydrophilic drugs, transporters located on the sinusoidal membrane are responsible for the hepatic uptake [1, 2]. Biliary excretion of many drags is also mediated by the primary active transporters, referred to as ATP-binding cassette transmembrane (ABC) transporters, located on the bile canalicular membrane [1, 3-5], Recently, many molecular biological... 

Suzuki, H., Sugiyama, Y., Transport of drugs across the hepatic sinusoidal membrane sinusoidal drug influx and efflux in the liver, Semin. Liver Dis. 2000, 20, 251-263. 

Laskin, D.L. and Gardner, C.R., Role of sinusoidal cells and inflammatory macrophages in hepatotoxicity, in Drug induced Liver Disease, Kaplowitz, N. and DeLeve, L, Eds., Marcel Dekker, New York, 2002, 183-211. 

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