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Neuroendocrine stress hormones do not recreate the postoperative hypercoagulable state
B A Rosenfeld1, N D Nguyen, I Sung
1Department of Anesthesiology/Critical Care Medicine, The Johns Hopkins University School of Medicine, Baltimore, Maryland, USA. brose@welchlink.welch.jhu.edu
Anesthesia and Analgesia
|March 12, 1998
Summary
Perioperative stress hormones do not cause a hypercoagulable state after surgery. Instead, infusions of epinephrine, cortisol, glucagon, angiotensin II, and vasopressin increased anticoagulants and fibrinolysis, suggesting they do not drive postoperative thrombosis.
Area of Science:
- Physiology
- Endocrinology
- Hematology
Background:
- Surgery induces a hypercoagulable state, increasing risks of arterial and venous thrombosis.
- The exact cause of this postoperative hypercoagulability remains unknown.
- Perioperative neuroendocrine changes are a leading hypothesis for this hemostatic alteration.
Purpose of the Study:
- To investigate the relationship between neuroendocrine hormones and hemostatic function.
- To determine if a specific cocktail of stress hormones contributes to postoperative hypercoagulability.
Main Methods:
- A double-blind, placebo-controlled, cross-over study involving 17 healthy volunteers.
- Intravenous infusion of a stress hormone cocktail (epinephrine, cortisol, glucagon, angiotensin II, vasopressin) for 24 hours.
- Measurement of hemostatic function via venous blood samples at baseline and 2, 8, and 24 hours post-infusion.
Main Results:
- No significant increases in hypercoagulability markers were observed.
- Elevated levels of tissue plasminogen activator and protein C activity were detected.
- These findings indicate a potential inhibition of coagulation and enhanced fibrinolysis.
Conclusions:
- Infusion of the studied stress hormones does not promote a hypercoagulable state in healthy individuals.
- The hormones increased fibrinolytic proteins and endogenous anticoagulants, counteracting coagulation.
- This suggests the investigated neuroendocrine stress hormones are unlikely to be the primary drivers of the postoperative hypercoagulable state.