Vagus nerve stimulation inhibits activation of coagulation and fibrinolysis during endotoxemia in rats

Background: Sepsis and endotoxemia are associated with concurrent activation of inflammation and the hemostatic mechanism, which both contribute to organ dysfunction and death. Electrical vagus nerve stimulation (VNS) has been found to inhibit tumor necrosis factor (TNF)‐α release during endotoxemia...

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Vydáno v:Journal of thrombosis and haemostasis Ročník 4; číslo 9; s. 1997 - 2002
Hlavní autoři: VAN WESTERLOO, D. J., GIEBELEN, I. A. J., MEIJERS, J. C. M., DAALHUISEN, J., DE VOS, A. F., LEVI, M., VAN DER POLL, T.
Médium: Journal Article
Jazyk:angličtina
Vydáno: Oxford, UK Blackwell Publishing Ltd 01.09.2006
Témata:
Animals
Blood Coagulation
coagulation
cytokines
Electric Stimulation
Electric Stimulation Therapy
Endotoxemia - pathology
Endotoxemia - therapy
endotoxin
Fibrinolysis
Inflammation - prevention & control
Interleukin-10 - analysis
Interleukin-6 - analysis
Kinetics
lipopolysaccharide
Lipopolysaccharides - administration & dosage
Male
Rats
Rats, Inbred Lew
Tumor Necrosis Factor-alpha - analysis
Vagus Nerve
ISSN:1538-7933, 1538-7836, 1538-7836
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Shrnutí:Background: Sepsis and endotoxemia are associated with concurrent activation of inflammation and the hemostatic mechanism, which both contribute to organ dysfunction and death. Electrical vagus nerve stimulation (VNS) has been found to inhibit tumor necrosis factor (TNF)‐α release during endotoxemia in rodents. Objective: To determine the effect of VNS on activation of coagulation and fibrinolysis. Methods: Rats received a sublethal i.v. dose of lipopolysaccharide (LPS) after electrical VNS or sham stimulation. Activation of coagulation and fibrinolysis, as well as cytokine release, was measured before LPS injection and 2, 4 and 6 h thereafter. Results: LPS induced activation of the coagulation system (increases in the plasma concentrations of thrombin–antithrombin complexes and D‐dimer, and a decrease in antithrombin) and biphasic changes in the fibrinolytic system [early rises of plasminogen activator activity and tissue‐type plasminogen activator, followed by a delayed increase in plasminogen activator inhibitor type 1 (PAI‐1)]. VNS strongly inhibited all LPS‐induced procoagulant responses and more modestly attenuated the fibrinolytic response. In addition, VNS attenuated the LPS‐induced increases in plasma and splenic concentrations of the proinflammatory cytokines TNF‐α and interleukin‐6 (IL‐6), while not influencing the release of the anti‐inflammatory cytokine IL‐10. Conclusion: These data illustrate a thus far unrecognized effect of VNS and suggest that the cholinergic anti‐inflammatory pathway not only impacts on inflammation but also on the coagulant‐anticoagulant balance.
Bibliografie:These authors contributed equally to this study.
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ISSN:1538-7933
1538-7836
1538-7836
DOI:10.1111/j.1538-7836.2006.02112.x