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Plasmin accelerates platelet-dependent prothrombinase formation without activating the platelets
L Liu1, J Freedman, A Hornstein
1Canadian Red Cross Society, Blood Services, Hamilton Ontario, Canada.
British Journal of Haematology
|February 1, 1996
Summary
Plasmin does not directly activate platelets or prothrombin. However, it potentiates thrombin-induced platelet activation and accelerates prothrombin activation, potentially explaining side effects of thrombolytic therapy.
Area of Science:
- Biochemistry
- Hematology
- Cardiovascular Research
Background:
- Thrombolytic therapy for myocardial infarction can lead to increased platelet activation and thrombosis.
- The precise mechanisms underlying these adverse effects require further investigation.
Purpose of the Study:
- To investigate whether plasmin, a key enzyme in thrombolysis, directly activates platelets and prothrombin.
- To elucidate plasmin's role in potentiating platelet activation and thrombin generation.
Main Methods:
- Experiments were conducted using recalcified platelet-rich plasma (RPRP) with varying concentrations of plasmin and inhibitors.
- Platelet activation markers (GMP-140, GP IIb-IIIa, GPIb) and prothrombin activation (prothrombin fragment 1 + 2) were measured.
- Prothrombin activation was also assessed in washed platelets under specific conditions with alpha-thrombin and factor Xa.
Main Results:
- Plasmin alone did not activate platelets or prothrombin in RPRP.
- Plasmin accelerated platelet activation, secretion, and prothrombin fragment 1 + 2 production in RPRP.
- Plasmin enhanced alpha-thrombin-induced platelet activation marker expression and potentiated prothrombin activation.
Conclusions:
- Plasmin does not directly activate platelets or prothrombin.
- Plasmin potentiates the platelet release reaction and enhances prothrombin activation, likely by increasing factor V availability.
- These findings suggest a mechanism contributing to thrombotic side effects observed after thrombolytic therapy.