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Volume 14, Issue 10 , Pages e857-e867 , October 2010

Pathogenesis of the hyperlipidemia of Gram-negative bacterial sepsis may involve pathomorphological changes in liver sinusoidal endothelial cells

Rajkumar Cheluvappa
- Department of Medicine, St. George Clinical School and Centre for Infection and Inflammation Research, School of Medical Sciences, Wallace Wurth Building, University of New South Wales, Gate 9 High Street, Sydney, NSW 2052, Australia
- Corresponding author. Tel.: +61 0406 0406 20; fax: +61 02 9385 1389.
Gerene M. Denning
- Department of Emergency Medicine, University of Iowa Hospitals and Clinics, Iowa City, Iowa, USA
Gee W. Lau
- Department of Pathobiology, College of Veterinary Medicine, University of Illinois at Urbana-Champaign, Urbana, Illinois, USA
Michael C. Grimm
- Department of Medicine, St. George Clinical School and Centre for Infection and Inflammation Research, School of Medical Sciences, Wallace Wurth Building, University of New South Wales, Gate 9 High Street, Sydney, NSW 2052, Australia
Sarah N. Hilmer
- Centre for Education and Research on Aging and ANZAC Research Institute, University of Sydney and Concord RG Hospital, Concord, New South Wales, Australia
- Departments of Aged Care and Clinical Pharmacology, Royal North Shore Hospital, St Leonards, New South Wales, Australia
David G. Le Couteur
- Centre for Education and Research on Aging and ANZAC Research Institute, University of Sydney and Concord RG Hospital, Concord, New South Wales, Australia

Received 8 May 2009 ,Revised 30 November 2009 ,Accepted 25 February 2010.

Hepatic microcirculation and the liver sinusoid. Structure of the liver sinusoid:¹⁸⁷ (A) Scanning electron micrograph of a vascular cast of the hepatic microcirculation and sinusoids showing a branch

Hepatic microcirculation and the liver sinusoid. Structure of the liver sinusoid:¹⁸⁷ (A) Scanning electron micrograph of a vascular cast of the hepatic microcirculation and sinusoids showing a branch of the portal vein (PV) and branch of the hepatic artery (HA) with surrounding sinusoidal microvascular network (S). A branch from the PV into the sinusoids is shown (↑). (B) Scanning electron micrograph of liver; Kupffer cell (KC) lying in a sinusoid. (C) Transmission electron micrograph of liver; the liver sinusoidal endothelial cell (LSEC) layer is thin and perforated with fenestrations (F). The extension of a stellate cell (HSC) lies beneath the liver sinusoidal endothelial cell.
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Probable pathogenesis of pseudomonal sepsis-related hyperlipidemia. Liver sinusoidal endothelial cell (LSEC) defenestration in bacterial/pseudomonal sepsis owing to toxins like pyocyanin or endotoxin

Probable pathogenesis of pseudomonal sepsis-related hyperlipidemia. Liver sinusoidal endothelial cell (LSEC) defenestration in bacterial/pseudomonal sepsis owing to toxins like pyocyanin or endotoxin (lipopolysaccharide) may exclude lipoproteins from the liver leading to lipoprotein retention in the peripheral vasculature accounting for bacterial/pseudomonal sepsis-related hyperlipidemia.
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