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Intermittent pneumatic foot compression can activate blood fibrinolysis without changes in blood coagulability and
1Department of Anesthesiology, Sapporo Medical University School of Medicine, South 1 West 16, Chuo-ku, Sapporo, Hokkaido 060-8543, Japan.
Acta Anaesthesiologica Scandinavica
|April 20, 2005
Summary
Intermittent pneumatic foot compression (IPC) activates blood fibrinolysis, increasing clot retraction and reducing thromboembolism risk. It does not affect blood coagulability or platelet function.
Area of Science:
- Vascular Surgery
- Thrombosis Research
- Biomedical Engineering
Background:
- Intermittent pneumatic foot compression (IPC) is a standard prophylaxis for peri-operative venous thromboembolism.
- Understanding IPC's precise effects on hemostasis is crucial for optimizing its clinical application.
- This study investigates IPC's impact on blood coagulation, fibrinolysis, and platelet function.
Purpose of the Study:
- To evaluate the effect of intermittent pneumatic foot compression (IPC) on blood coagulation and fibrinolysis.
- To assess IPC's influence on platelet function.
- To measure serum levels of key hemostatic markers including tissue-type plasminogen activator (t-PA), thrombomodulin (TM), and activated protein C (APC).
Main Methods:
- Eight subjects underwent 60-minute IPC (130 mmHg, 0.3 Hz interval).
- Blood coagulation and fibrinolysis were assessed using a Sonoclot whole blood analyzer.
- Platelet function was measured with a platelet aggregation monitor (WBA analyzer™), alongside serum t-PA, TM, and APC levels.
Main Results:
- IPC significantly shortened Sonoclot time-to-peak and increased clot retraction rate, indicating enhanced fibrinolysis.
- Platelet aggregatory threshold index (PATI) remained unchanged, showing no direct activation of platelet function by IPC.
- Serum t-PA concentration decreased significantly, suggesting a mechanism for fibrinolytic activation; other humoral parameters were unaffected.
Conclusions:
- IPC effectively activates blood fibrinolysis, contributing to its prophylactic role against thromboembolism.
- The mechanism involves enhanced fibrinolytic activity, potentially via t-PA function modulation, rather than direct effects on coagulation or platelet aggregation.
- IPC is beneficial for thromboembolism prophylaxis by promoting fibrinolysis and inhibiting blood stasis.