Effects of sympathetic activation by adrenergic infusions on hemostasis invivo

Overactivity of the sympathetic nervous system (SNS) has been related to in creased cardiovascular morbidity. Historical reports suggest hastening of b lood coagulation following intravenous administration of epinephrine. Given the important role of the hemostatic System in atherosclerosis and thrombo sis, it is surprising that short-term adrenergic effects on blood coagulati on, fibrinolysis and platelet activity have not been scrutinized closely. T o elucidate such effects in vivo, this paper reviews human studies in which alpha- and beta -sympathomimetic agents had been infused. The literature s uggests a dose-dependent stimulation of factor VIII clotting activity, von Willebrand factor antigen, tissue-type plasminogen activator, and platelets within a 15- to 40-min infusion of epinephrine. Precise mechanisms underly ing hemostatic changes with sympathetic activation remain to some extent sp eculative. However, there is evidence from adrenoreceptor blockade studies that coagulation and fibrinolysis molecules are released into circulation b y stimulation of vascular endothelial beta -adrenoreceptors (most likely be ta2-receptors). Combined alpha2- and beta2-adrenoreceptor-related mechanism (s) are responsible for platelet activation. Short-term activation of the S NS effects regular hemostatic activity. While in healthy individuals the he mostatic balance between coagulation and fibrinolysis may be preserved, cat echolamine surge may trigger a hypercoagulable state and enhance the odds o f overt thrombosis in patients with atherosclerotic disease.