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Experimental endotoxemia induces leukocyte adherence and plasma extravasation within the rat pial microcirculation
J. Zhou, M. Schmidt, B. Johnston, F. Wilfart, S. Whynot, O. Hung, M. Murphy, V. Černý, D. Pavlovic, C. Lehmann
Language English Country Czech Republic
Document type Research Support, Non-U.S. Gov't
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- MeSH
- Cell Adhesion MeSH
- Endothelium, Vascular metabolism physiopathology MeSH
- Endotoxemia metabolism physiopathology MeSH
- Interferon-gamma blood MeSH
- Interleukin-1beta blood MeSH
- Interleukin-6 blood MeSH
- Capillary Permeability MeSH
- Rats MeSH
- Leukocytes physiology MeSH
- Microvessels metabolism physiopathology MeSH
- Microcirculation physiology MeSH
- Brain blood supply MeSH
- Cerebral Veins metabolism MeSH
- Rats, Inbred Lew MeSH
- Tumor Necrosis Factor-alpha blood MeSH
- Animals MeSH
- Check Tag
- Rats MeSH
- Male MeSH
- Animals MeSH
- Publication type
- Research Support, Non-U.S. Gov't MeSH
Disturbance of capillary perfusions due to leukocyte adhesion, disseminated intravascular coagulation, tissue edema is critical components in the pathophysiology of sepsis. Alterations in brain microcirculation during sepsis are not clearly understood. The aim of this study is to gain an improved understanding of alterations through direct visualization of brain microcirculations in an experimental endotoxemia using intravital microscopy (IVM). Endotoxemia was induced in Lewis rats with Lipopolysaccharide (LPS, 15 mg/kg i.v.). The dura mater was removed via a cranial window to expose the pial vessels on the brain surface. Using fluorescence dyes, plasma extravasation of pial venous vessels and leukocyte-endothelial interaction were visualized by intravital microscopy 4 h after LPS administration. Plasma cytokine levels of IL1-β, IL-6, IFN-γ, TNF-α and KC/GRO were evaluated after IVM. A significant plasma extravasation of the pial venous vessels was found in endotoxemia rats compared to control animals. In addition, a significantly increased number of leukocytes adherent to the pial venous endothelium was observed in septic animals. Endotoxemia also induced a significant elevation of plasma cytokine levels of IL1-β, IL-6, IFN-γ, TNF-α and KC/GRO. Endotoxemia increased permeability in the brain pial vessels accompanied by an increase of leukocyte-endothelium interactions and an increase of inflammatory cytokines in the plasma.
Department of Pathophysiology American School of Medicine European University Belgrade Serbia
Departments Microbiology and Imunology Pediatrics Pathology Dalhousie University Halifax NS Canada
Departments of Anasthesia Biomedical Engineering Dalhousie University Halifax NS Canada
Departments of Anasthesia Dalhousie University Halifax NS Canada
Departments of Anasthesia Pharmacology Dalhousie University Halifax NS Canada
Departments of Anesthesia Microbiology and Immunology Dalhousie University Halifax NS Canada
References provided by Crossref.org
Literatura
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- $a Disturbance of capillary perfusions due to leukocyte adhesion, disseminated intravascular coagulation, tissue edema is critical components in the pathophysiology of sepsis. Alterations in brain microcirculation during sepsis are not clearly understood. The aim of this study is to gain an improved understanding of alterations through direct visualization of brain microcirculations in an experimental endotoxemia using intravital microscopy (IVM). Endotoxemia was induced in Lewis rats with Lipopolysaccharide (LPS, 15 mg/kg i.v.). The dura mater was removed via a cranial window to expose the pial vessels on the brain surface. Using fluorescence dyes, plasma extravasation of pial venous vessels and leukocyte-endothelial interaction were visualized by intravital microscopy 4 h after LPS administration. Plasma cytokine levels of IL1-β, IL-6, IFN-γ, TNF-α and KC/GRO were evaluated after IVM. A significant plasma extravasation of the pial venous vessels was found in endotoxemia rats compared to control animals. In addition, a significantly increased number of leukocytes adherent to the pial venous endothelium was observed in septic animals. Endotoxemia also induced a significant elevation of plasma cytokine levels of IL1-β, IL-6, IFN-γ, TNF-α and KC/GRO. Endotoxemia increased permeability in the brain pial vessels accompanied by an increase of leukocyte-endothelium interactions and an increase of inflammatory cytokines in the plasma.
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