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© The Rockefeller University Press, 0022-1007/1997/3/1143/ $5.00
The Journal of Experimental Medicine, Volume 185, Number 6, March 17, 1997 1143-1148

Brief Definitive Reports

Epinephrine Exerts Anticoagulant Effects during Human Endotoxemia

Tom van der Poll*,{ddagger}, Marcel Levi{ddagger},§, Mieke Dentener||, Patty M. Jansen**, Susette M. Coyle*, Carla C. Braxton*, Wim A. Buurman, C. Erik Hack**, Jan W. ten Cate§, and Stephen F. Lowry*,¶

From * Cornell University Medical College, Laboratory of Surgical Metabolism, Department of Surgery, New York 10021; {ddagger} Academic Medical Center, Department of Internal Medicine and § The Center of Hemostasis, Thrombosis, Atherosclerosis, and Inflammation Research, University of Amsterdam, 1105 AZ Amsterdam, The Netherlands; || Department of Pulmonology and Department of Surgery, University of Limburg, 6200 MD Maastricht, The Netherlands; ** Department of Autoimmune Diseases, Central Laboratory of The Netherlands Red Cross Blood Transfusion Service, Amsterdam, 1105A2 The Netherlands

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-{alpha}2–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.

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.


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