Epinephrine exerts anticoagulant effects during human endotoxemia
To determine the effect of a physiologically relevant elevation in the plasma concentrations of epinephrine on the activation of the hemostatic mechanism during endotoxemia, 17 healthy men were studied after intravenous injection of lipopolysaccharide (LPS, 2 ng/kg), while receiving a continuous inf...
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Published in | The Journal of experimental medicine Vol. 185; no. 6; pp. 1143 - 1148 |
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Main Authors | , , , , , , , , , |
Format | Journal Article |
Language | English |
Published |
United States
The Rockefeller University Press
17.03.1997
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Subjects | |
Online Access | Get full text |
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Summary: | To determine the effect of a physiologically relevant elevation in the plasma concentrations of epinephrine on the activation of the hemostatic mechanism during endotoxemia, 17 healthy men were studied after intravenous injection of lipopolysaccharide (LPS, 2 ng/kg), while receiving a continuous infusion of epinephrine (30 ng/kg/min) started either 3 h (n = 5) or 24 h (n = 6) before LPS injection, or an infusion of normal saline (n = 6). Activation of the coagulation system (plasma concentrations of thrombin-antithrombin III complexes and prothrombin fragment F1+2) was significantly attenuated in the groups treated with epinephrine when compared with subjects injected with LPS only (P <0.05). Epinephrine enhanced LPS-induced activation of fibrinolysis (plasma levels of tissue-type plasminogen activator and plasmin-alpha2-antiplasmin complexes; P <0.05), but did not influence inhibition of fibrinolysis (plasminogen activator inhibitor type I). In subjects infused with epinephrine, the ratio of maximal activation of coagulation and maximal activation of fibrinolysis was reduced by >50%. Hence, epinephrine exerts antithrombotic effects during endotoxemia by concurrent inhibition of coagulation, and stimulation of fibrinolysis. Epinephrine, whether endogenously produced or administered as a component of treatment, may limit the development of disseminated intravascular coagulation during systemic infection. |
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Bibliography: | ObjectType-Article-2 SourceType-Scholarly Journals-1 ObjectType-Feature-1 content type line 23 Address correspondence to Stephen F. Lowry, M.D., University of Medicine & Dentistry of New Jersey, Robert Wood Johnson Medical School, Department of Surgery, One Robert Wood Johnson Place–CN19, New Brunswick, NJ 08903-0019. |
ISSN: | 0022-1007 1540-9538 |
DOI: | 10.1084/jem.185.6.1143 |