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Pathophysiology of Lymphatic Insufficiency and Principles of Treatment
Published in Waldemar L. Olszewski, Lymph Stasis: Pathophysiology, Diagnosis and Treatment, 2019
Charles L. Witte, Marlys H. Witte
Because the lining of the hepatic sinusoid is discontinuous, edema of the liver is invariably protein-rich whatever the inciting cause (circulatory congestion from hepatic venous outflow block, viral infection, or drug toxicity). When hepatic interstitial edema persists either from high (i.e., overproduction) or low (stagnation) output failure of regional lymph flow, bundles of collagen accumulate particularly in Disse’s space and defenestration of the endothelium takes place forming a pathological basement membrane (i.e., capillarization).27–29 Disorders as disparate as Budd-Chiari syndrome, alcohol abuse, chronic viral hepatitis, exposure to vinyl chloride, and vitamin A toxicity, therefore, are associated alike with widespread desmoplasia and in the extreme, frank cirrhosis.
Liver, Gallbladder, and Exocrine Pancreas
Published in Pritam S. Sahota, James A. Popp, Jerry F. Hardisty, Chirukandath Gopinath, Page R. Bouchard, Toxicologic Pathology, 2018
Russell C. Cattley, James A. Popp, Steven L. Vonderfecht
Residing along the intravascular surface of the hepatic sinusoids are the Kupffer cells, which are phagocytic cells that share common lineage and many characteristics with monocytes derived from the bone marrow (Klein et al. 2007). These cells are activated by opsonized and particulate materials in the circulation, produce cytokines, and locally by phagocytosis, which can perpetuate injury and/or remove necrotic tissue.
Clinical pharmacology (and toxicology and therapeutics)
Published in Shibley Rahman, Avinash Sharma, A Complete MRCP(UK) Parts 1 and 2 Written Examination Revision Guide, 2018
Shibley Rahman, Avinash Sharma
In the chronic state, cirrhosis of any aetiology, viral hepatitis and hepatoma can decrease drug metabolism. In moderate to severe liver dysfunction, rates of drug metabolism may be reduced by as much as 50%. The mechanism is thought to be due to spatial separation of blood from the hepatocyte by fibrosis along the hepatic sinusoids.
Morphological, biochemical, and histopathological effects of levetiracetam on pregnant albino rats and their offspring
Published in Ultrastructural Pathology, 2023
Safaa M. H. Abdelaziz, Ranya Mohammed Abdelgalil, Shaimaa R. Abdelmohsen
H–E stained liver sections of IA and IIA subgroup mothers revealed no significant histological changes. The liver was found to be made up of hepatocytes arranged in branching and interconnected cords emanating from the central vein and interposed with the hepatic sinusoids (Figure 1A). The hepatocytes have a polyhedral form. Their cytoplasm was granular and eosinophilic, and their nuclei were vesicular basophilic with one or two vesicular nucleoli (Figures 1A and 1D). Flat endothelial cells and von Kupffer cells lined the blood sinusoids, which appeared slit-shaped between the hepatic cords (Figures 1A and 1D). A branch of the portal vein, a branch of the hepatic artery, a branch of the bile duct, and a lymph vessel were all found in the portal tracts (Figure 1D). The distribution of tiny collagen fibers around the central vein and elements of the portal tract was revealed by Masson’s trichrome staining (Figure 2A, 2D).
Flavonoid-rich fraction of Lasianthera africana leaves alleviates hepatotoxicity induced by carbon tetrachloride in Wistar rats
Published in Drug and Chemical Toxicology, 2022
Daniel Emmanuel Ekpo, Parker Elijah Joshua, Arome Solomon Odiba, Okwesilieze Fred Chiletugo Nwodo
In the curative study, rat liver; post-treated with 3 mg/kg b.w. LAFRF (group 7) showed slightly shrunken and irregular shaped cells (blue arrow) consistent with early stage apoptosis. Normal hepatocytes (black arrow) are present (Figure 6(G)). Photomicrograph of liver in group 8, post-treated with 10 mg/kg b.w. LAFRF showed a typical portal tract containing three main structures; portal venules (PV) characterized by a thin wall lined by endothelial cells, smaller diameter thick-walled vessels which are terminal branches of hepatic artery (HA), and bile ductile (BD) are observed. Meanwhile, surrounding the portal tract are anastomosing plates of hepatocytes (H), between which are the hepatic sinusoids (S) receiving blood from the hepatic portal and hepatic arterial systems (Figure 6(H)). Photomicrograph of liver tissue of group 9 rats treated with 30 mg/kg b.w. LAFRF following CCl4-intoxication showed presence of cytoplasmic vacuolation (black arrow), with visible normal hepatocytes (blue arrow) (Figure 6(I)). Histomorphology of group 10 rat liver, post-treated with 100 mg/kg b.w. L-ascorbic acid showed diffused micro vesicles (MV) (white arrow), with passive spotty hemorrhage (PSH) (blue arrow) observed (Figure 6(J)).
Progress in research on the roles of TGR5 receptor in liver diseases
Published in Scandinavian Journal of Gastroenterology, 2021
Ke Ma, Dan Tang, Chang Yu, Lijin Zhao
Portal hypertension is one of the most important complications of chronic liver disease caused by increased intrahepatic vascular resistance in hepatic fibrosis, microvascular thrombosis, hepatic sinusoid endothelial cell dysfunction, HSC activation, and platelet dysfunction [13]. The manifestations of limbal epithelial stem cell (LESC) dysfunction include decreased permeability and decreased nitric oxide (NO) secretion. In the physiological state, LESCs have high permeability, whereas in chronic liver disease, liver fibrosis causes LESCs to lose fenestration and form a basement membrane, causing a decrease in permeability. As an important vasodilator, a decrease in NO secretion significantly increases intravascular pressure. Notably, TGR5 is highly expressed in LSECs. When TGR5 is activated, it induces the expression and activation of endothelial nitric oxide synthase (eNOS) in endothelial cells, and NO secretion mainly depends on the activity and expression of eNOS [107]. In addition, the activation of TGR5 can trigger the expression of cystathionine-gamma-lyase (CSE) and the serine phosphorylation of eNOS, leading to the production of hydrogen sulphide (H2S) and NO, respectively. Consequently, this inhibits the expression and secretion of the strong vasoconstrictor ET-1 in LSECs (Figure 2) [107–111].