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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| Published in: | Journal of thrombosis and haemostasis Vol. 4; no. 9; pp. 1997 - 2002 |
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| Main Authors: | , , , , , , |
| Format: | Journal Article |
| Language: | English |
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Oxford, UK
Blackwell Publishing Ltd
01.09.2006
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| ISSN: | 1538-7933, 1538-7836, 1538-7836 |
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| Abstract | 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. |
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| AbstractList | 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. 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)-alpha release during endotoxemia in rodents. To determine the effect of VNS on activation of coagulation and fibrinolysis. 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. 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-alpha and interleukin-6 (IL-6), while not influencing the release of the anti-inflammatory cytokine IL-10. 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. 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)-alpha release during endotoxemia in rodents.BACKGROUNDSepsis 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)-alpha release during endotoxemia in rodents.To determine the effect of VNS on activation of coagulation and fibrinolysis.OBJECTIVETo determine the effect of VNS on activation of coagulation and fibrinolysis.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.METHODSRats 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.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-alpha and interleukin-6 (IL-6), while not influencing the release of the anti-inflammatory cytokine IL-10.RESULTSLPS 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-alpha and interleukin-6 (IL-6), while not influencing the release of the anti-inflammatory cytokine IL-10.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.CONCLUSIONThese 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. |
| Author | LEVI, M. GIEBELEN, I. A. J. DE VOS, A. F. DAALHUISEN, J. VAN DER POLL, T. VAN WESTERLOO, D. J. MEIJERS, J. C. M. |
| Author_xml | – sequence: 1 givenname: D. J. surname: VAN WESTERLOO fullname: VAN WESTERLOO, D. J. – sequence: 2 givenname: I. A. J. surname: GIEBELEN fullname: GIEBELEN, I. A. J. – sequence: 3 givenname: J. C. M. surname: MEIJERS fullname: MEIJERS, J. C. M. – sequence: 4 givenname: J. surname: DAALHUISEN fullname: DAALHUISEN, J. – sequence: 5 givenname: A. F. surname: DE VOS fullname: DE VOS, A. F. – sequence: 6 givenname: M. surname: LEVI fullname: LEVI, M. – sequence: 7 givenname: T. surname: VAN DER POLL fullname: VAN DER POLL, T. |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/16805873$$D View this record in MEDLINE/PubMed |
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| Snippet | Background: Sepsis and endotoxemia are associated with concurrent activation of inflammation and the hemostatic mechanism, which both contribute to organ... Sepsis and endotoxemia are associated with concurrent activation of inflammation and the hemostatic mechanism, which both contribute to organ dysfunction and... |
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| SubjectTerms | 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 |
| Title | Vagus nerve stimulation inhibits activation of coagulation and fibrinolysis during endotoxemia in rats |
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