NEUROENDOCRINE STRESS HORMONES DO NOT RECREATE THE POSTOPERATIVE HYPERCOAGULABLE STATE

Surgery causes changes in hemostasis, leading to a hypercoagulable sta te that has been linked to both arterial and venous thrombotic complic ations. The etiology of this state is unknown, but many investigators have hypothesized that perioperative neuroendocrine changes are respon sible. 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 IV (epinephrine, cortisol, glucagon, angiotens in II, and vasopressin) for 24 h in a blind, placebo-controlled, cross -over design in our clinical research center. Venous blood samples wer e obtained for measurement of hemostatic function before the infusion and at 2, 8, and 24 h. There were no demonstrable increases in any mea sure of hypercoagulability. Alternatively, there was an increase in ti ssue plasminogen activator and protein C activity. These changes are c onsistent with an inhibition of coagulation and improved fibrinolysis. These data suggest that this combination of neuroendocrine hormones i s not responsible for the postoperative hypercoagulable state. Implica tions: Infusion of five stress hormones (epinephrine, cortisol, glucag on, vasopressin, and angiotensin II) to normal volunteers does not cau se increases in procoagulant proteins and platelet reactivity or decre ases in fibrinolytic proteins Alternatively, these five hormones cause d increased levels of fibrinolytic proteins (tissue plasminogen activa tor) and endogenous anticoagulants (protein C antigen and activity).