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Determination of the Procoagulant Activity of Extracellular Vesicle (EV) Using EV-Activated Clotting Time (EV-ACT)
Published on: August 4, 2023
Hypercoagulability in response to elevated body temperature and central hypovolemia.
Martin A S Meyer1, Sisse R Ostrowski, Anders Overgaard
1Section for Transfusion Medicine, Capital Regional Blood Bank, Copenhagen University Hospital, Rigshospitalet, Copenhagen, Denmark; Center for Translational Injury Research, Department of Surgery, University of Texas Health Science Center at Houston, Houston, Texas.
The Journal of Surgical Research
|July 17, 2013
Summary
Elevated body temperature and reduced central blood volume (CBV) in healthy volunteers induced hypercoagulability, evidenced by shortened clotting times and increased D-dimer. This suggests a link between heat stress, hypovolemia, and clotting activation in critical illness.
Area of Science:
- Physiology
- Hemostasis
- Critical Care Medicine
Background:
- Coagulation abnormalities are linked to adverse outcomes in critically ill patients.
- Trauma patients in hot environments experience systemic inflammation, fever, and reduced central blood volume (CBV), alongside hemostatic changes and endothelial damage.
Purpose of the Study:
- To investigate the independent effects of experimentally elevated body temperature and reduced CBV on hemostasis and endothelial activation.
Main Methods:
- Eleven healthy volunteers underwent heat stress to increase core temperature.
- Lower body negative pressure (LBNP) was used for progressive CBV reduction.
- Hemostasis was assessed using whole blood assays, hematologic tests, and plasma biomarkers of coagulation and endothelial activation.
Main Results:
- Elevated body temperature and decreased CBV significantly activated coagulation, indicated by shortened activated partial thromboplastin time and altered thrombelastography parameters (P < 0.05).
- Increased fibrinolysis was observed, with a significant rise in D-dimer levels (P = 0.016).
- Plasma levels of adrenaline and noradrenaline markedly increased (P < 0.006).
Conclusions:
- Experimental elevation of body temperature and reduction of CBV induce a state of hypercoagulability in healthy individuals.
- No significant endothelial activation or damage was detected under these experimental conditions.
- These findings suggest that elevated body temperature and reduced CBV may contribute to hypercoagulability in critically ill patients, potentially mediated by sympathetic activation.
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