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From * Cornell University Medical College, Laboratory of Surgical Metabolism, Department of
Surgery, New York 10021; 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- 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
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.
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