title: Neuroendocrine stress hormones do not recreate the postoperative hypercoagulable state.
abstract: Surgery causes changes in hemostasis, leading to a hypercoagulable state that has been linked to both arterial and venous thrombotic complications. The etiology of this state is unknown, but many investigators have hypothesized that perioperative neuroendocrine changes are responsible. We have previously demonstrated minimal increases in hemostatic function with a stress hormone infusion. This study was undertaken to further examine the relationship between neuroendocrine hormones and hemostatic function. Seventeen healthy volunteers were administered a stress hormone cocktail i.v. (epinephrine, cortisol, glucagon, angiotensin II, and vasopressin) for 24 h in a blind, placebo-controlled, cross-over design in our clinical research center. Venous blood samples were obtained for measurement of hemostatic function before the infusion and at 2, 8, and 24 h. There were no demonstrable increases in any measure of hypercoagulability. Alternatively, there was an increase in tissue plasminogen activator and protein C activity. These changes are consistent with an inhibition of coagulation and improved fibrinolysis. These data suggest that this combination of neuroendocrine hormones is not responsible for the postoperative hypercoagulable state.
  
  
  CONCLUSIONS
  Infusion of five stress hormones (epinephrine, cortisol, glucagon, vasopressin, and angiotensin II) to normal volunteers does not cause increases in procoagulant proteins and platelet reactivity or decreases in fibrinolytic proteins. Alternatively, these five hormones caused increased levels of fibrinolytic proteins (tissue plasminogen activator) and endogenous anticoagulants (protein C antigen and activity).
authors.affiliation: Department of Anesthesiology/Critical Care Medicine, The Johns Hopkins University School of Medicine, Baltimore, Maryland, USA. brose@welchlink.welch.jhu.edu
authors.forename: B A
authors.initials: BA
authors.lastname: Rosenfeld
authors.forename: N D
authors.initials: ND
authors.lastname: Nguyen
authors.forename: I
authors.initials: I
authors.lastname: Sung
authors.forename: N
authors.initials: N
authors.lastname: Faraday
mesh_terms: D000328:Adult; D000804:Angiotensin II / Q000494:pharmacology; D001777:Blood Coagulation / Q000187:drug effects*; D004837:Epinephrine / Q000494:pharmacology; D005260:Female; D005934:Glucagon / Q000494:pharmacology; D006439:Hemodynamics / Q000187:drug effects; D006801:Humans; D006854:Hydrocortisone / Q000494:pharmacology; D006943:Hyperglycemia / Q000139:chemically induced; D007958:Leukocyte Count; D008297:Male; D009638:Norepinephrine / Q000494:pharmacology; D017395:Plasminogen Activator Inhibitor 1 / Q000097:blood; D010976:Platelet Count / Q000187:drug effects; D011184:Postoperative Period; D011486:Protein C / Q000378:metabolism; D013312:Stress, Physiological / Q000097:blood; D013997:Time Factors; D010959:Tissue Plasminogen Activator / Q000097:blood; D014667:Vasopressins / Q000494:pharmacology
chemical_list: D017395:Plasminogen Activator Inhibitor 1; D011486:Protein C; D014667:Vasopressins; D000804:Angiotensin II; D005934:Glucagon; D010959:Tissue Plasminogen Activator; D006854:Hydrocortisone; D009638:Norepinephrine; D004837:Epinephrine