Periportal cells

Figure 8.30 Different roles of periportal and perivenous cells in the liver in respect of glutamine metabolism. Glutamine is converted to glucose in periportal cells via gluconeogenesis in perivenous cells, ammonia is taken up, to form glutamine, which is released into the blood. This emphasises the importance of the liver in removing ammonia from the blood, i.e. if possesses two process to ensure that all the ammonia is removed.

The liver is unusual in that it receives blood from two sources, the hepatic artery and the hepatic portal vein. The two supplies eventually join at the central vein, hence hepatocytes are of two types those which are exposed to blood derived largely from the hepatic artery, known as the perivenons cells, and those that are exposed to blood largely from the portal vein which are known as periportal cells (see Chapter 8). The periportal hepatocytes contain the enzymes of the ornithine cycle. In contrast, the... 

This compartmentation of processes in the liver cells occurs with other pathways glycolysis occurs mainly in the perivenous cells whereas gluconeogenesis occurs mainly in the periportal cells (Chapter 6). 

The presence of elevated plasma B, in the presence of normal AST could be explained by the lobular distribution of the enzymes since AST is mainly in periportal cells and alcohol damages centrilobular cells that are rich in B, but not AST (R2). The explanation for the converse finding of normal B, in the presence of a raised AST is less clear. This pattern of results could occur if cellular necrosis... 

E. histolytica invades mucosal cells of colonic epithelium, producing the classic flask-shaped ulcer in the submucosa. The trophozoite toxin has a cytocidal effect on cells. If the trophozoite gets into the portal circulation, it will be carried to the liver, where it produces abscess and periportal fibrosis. Liver abscesses are more common in men than women and are rarely seen in children. Amebic ulcerations can affect the perineum and genitalia, and abscesses may occur in the lung and brain. 

Findings from studies of schistosomiasis-induced liver fibrosis, as well as other models of pulmonary, kidney, and liver fibrosis, strongly support the role of CD4+ Th2 cells in the progression of fibrosis (4). In this regard, analyses of gene and protein expression after stimulation by Thl (vs. Th2) cytokines indicates that IL-4 is found at increased concentrations in the bronchoalveolar lavage (BAL) fluid of patients with idiopathic pulmonary fibrosis, as well as in the peripheral blood mononuclear cells of those afflicted with periportal fibrosis (10,53-56). 

The next largest pool is the liver [26], where the highest concentration is found in the periportal areas. Other organs in which mercury is likely to accumulate are the mucous membranes, the epithelium of the skin, the spleen, the interstitial cells of the testicles, and some parts of the brain. 

Fitzhugh and Nelson (19) found that oxalic acid up to 1.2% of the diet did not affect growth or mortality rate of rats fed oxalic acid for 1 year. Microscopic pathological examination showed no major visceral damage, but some of the rats showed slight periportal hypertrophy of the hepatic cells along with slight centrolobular atrophy. 

Hadassah bred) Hepatic 29 (scattered hemorrhagic areas of necrosis, increased ALT, degeneration of hepatocytes, periportal infiltration with inflammatory cells, microthrombi in portal veins) 1972... 

Benzene is metabolized primarily in the liver by the cytochrome P-450 system (Parke 1989). It appears that the metabolism of benzene by the hepatic cytochrome P-450 system plays an important role in its bioactivation and toxicity. Sammett et al. (1979) provided corroborative evidence of this by showing that partial hepatectomy of rats diminished both the rate of metabolism of benzene and its toxicity. An increase in altered hepatic foci has been shown in male rats after benzene exposure in conjunction with initiator and promotor administration (Dragan et al. 1993). A dose of 500 mg/kg of benzene administered subcutaneously once daily, 5 days a week for 26 weeks to Wistar rats resulted in focal fine droplet fatty metamorphosis with accompanying lymphoidal infiltration in the liver after 12 weeks (Bloch et al. 1990). In some cases a proliferated histocyte-like cells formed clusters in the vicinity of the periportal fields. After 26 weeks, more diffuse steatosis, feathery degeneration of hepatocytes, single necrotic cells were seen. 

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