Lipopolysaccharide endotoxin model

Another model that is also used widely in rats and mice is a model of systemic thrombosis or disseminated intravascular coagulation (DIC), which is induced by tissue factor, endotoxin (lipopolysaccharide), or FXa (Herbert et al. 1996 Yamazaki et al. 1994 Sato et al. 1998). After systemic administration of the thrombogenic stimulus, this model can be performed with or without mechanical vena caval stasis. When stasis is used, the major parameter is the thrombus mass, but when stasis is not used, the readouts are... 

A primary mediator that was demonstrated to participate in meningitis-induced BBB dismption is nitric oxide (NO). NO is produced in response to exposure to bacterial endotoxins by the host endothelial cells. In an animal model of lipopolysaccharide-induced meningitis, BBB dismption and NO production sites in the brain co-local-ized, and NO-synthase inhibitors reduced the meningeal-associated alterations in BBB permeability. NO is likely produced by astrocytes, and it decreases endothe-lin-1 secretion by brain microvessel endothelial cells. ... 

Weber and coworkers were able to show in an in vitro model, that endotoxin adsorption depends both, on chemical composition and the manufacturing process of the membrane [30], In fact, hydrophobic parts of the lipopolysaccharide molecule (LPS, endotoxin) are considered to interact with hydrophobic entities within the pol-ysulfone structure thereby facilitating their removal [29] (Tables 13.3 and 13.4). 

Urinary bladder. Kreft and coworkers (Kreft, Romih et al. 2002) established an in vitro culture model that closely resembles whole mouse urothelial tissue. When examined at the ultrastructural level, the cultured urothelium was polarized and organized as a multilayered epithelium, and epithelial organization was stabilized by well developed cell junctions. Desquamation of urinary bladder epithelial cells can be induced by constant illumination for 96 hours or by application of endotoxin lipopolysaccharide. Cell detachment involves interruption of TJ between neighbouring cells (Jezemik 1996). Urothelium permeability was studied in an experimental ischemic model of mouse urinary bladder by means of lanthanum nitrate tracer (Korosec and Jezemik 2000). Ischemia induces breakdown of the blood-urine permeability barrier by dismption of the TJ. 

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