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Updated: Aug 12, 2026
10:10
Platelet Adhesion and Aggregation Under Flow using Microfluidic Flow Cells
Published on: October 27, 2009
Tissue-type plasminogen activator and streptokinase induce platelet hyperaggregability in the rabbit
Thrombosis Research
|May 15, 1987
Summary
Thrombolytic therapy with tissue plasminogen activator (t-PA) or streptokinase (SK) can cause hyperaggregable platelets. This platelet response may contribute to blood vessel reocclusion after successful recanalization.
Area of Science:
- Cardiovascular Science
- Hematology
- Pharmacology
Background:
- Thrombolytic agents like tissue plasminogen activator (t-PA) and streptokinase (SK) are crucial for dissolving blood clots.
- Understanding the impact of these therapies on platelet function is essential for managing potential complications.
Purpose of the Study:
- To investigate the effects of in vivo thrombolytic therapy with t-PA and SK on ex vivo platelet aggregability in rabbits.
- To determine if thrombolytic agents induce platelet hyperaggregability and affect circulating platelet counts.
Main Methods:
- Rabbits were treated in vivo with different doses of t-PA (10 and 30 micrograms/kg/min) or SK.
- Ex vivo platelet aggregation was assessed using collagen, arachidonic acid, and ADP as agonists.
- Circulating platelet counts were measured after treatment.
Main Results:
- Both t-PA and SK induced significant ex vivo platelet hyperaggregability in response to various agonists.
- t-PA treatment led to a notable decrease in circulating platelet counts.
- SK infusion also resulted in enhanced platelet aggregation.
Conclusions:
- Thrombolytic therapy with t-PA and SK can lead to a state of platelet hyperaggregability.
- This induced platelet hyperaggregability may be a contributing factor to the reocclusion of blood vessels previously opened by thrombolysis.
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