title: Endotoxin-induced arterial endothelial barrier dysfunction assessed by an in vitro model.
abstract: Using an in vitro model in which albumin transfer across monolayers of bovine aortic endothelial cells (BAEC) was measured, we have shown that lipopolysaccharide (LPS) induces a concentration-dependent increase in endothelial permeability. This increase was biphasic, having an early peak at 2 h and rising again by 24 h. Both peaks were abolished by polymixin B (PMB) but were unaffected by N omega-monomethyl-L-arginine, N omega-nitro-L-arginine methyl ester or dexamethasone. Furthermore, LPS did not stimulate nitric oxide production by BAEC following 24 h exposure. Thus, the LPS-induced increase in permeability may account for the vascular leakage of septic shock, but the L-arginine-nitric oxide system does not appear to be involved.
authors.affiliation: Department of Pharmacology, University of Glasgow.
authors.forename: R S
authors.initials: RS
authors.lastname: Berman
authors.forename: J D
authors.initials: JD
authors.lastname: Frew
authors.forename: W
authors.initials: W
authors.lastname: Martin
mesh_terms: D000418:Albumins / Q000378:metabolism; D000818:Animals; D002199:Capillary Permeability / Q000187:drug effects; D002417:Cattle; D002478:Cells, Cultured; D004305:Dose-Response Relationship, Drug; D004730:Endothelium, Vascular / Q000187:drug effects* / Q000378:metabolism; D008070:Lipopolysaccharides / Q000633:toxicity*; D009569:Nitric Oxide / Q000502:physiology; D012772:Shock, Septic / Q000378:metabolism
chemical_list: D000418:Albumins; D008070:Lipopolysaccharides; D009569:Nitric Oxide