Key result
Released ADP stabilizes thrombin-induced platelet aggregates, preventing their deaggregation by inhibitors.
Why the study?
The role of released ADP in stabilizing thrombin-induced human platelet aggregates and its mechanism of action was unclear.
Population
Normal human platelets, delta-storage pool deficiency platelets, and platelets from a patient with ADP sensitivity impairment
Comparison
Thrombin-induced aggregation with and without inhibitors and exogenous ADP or other agents
Design
Preclinical experimental study
Authors
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May guide ADP-targeted antiplatelet development; leaves open translation from in vitro aggregates to clinical thrombosis.
This in vitro study demonstrates that released ADP plays a specific and crucial role in stabilizing thrombin-induced human platelet aggregates.
Cattaneo et al. (1990) studied delta-storage pool deficiency. Adenosine diphosphate (ADP) vs. Control platelets / no ADP was evaluated on Platelet deaggregation response to hirudin, chymotrypsin, and PGE1. Released ADP stabilizes thrombin-induced human platelet aggregates, preventing their deaggregation by inhibitors, whereas platelets lacking releasable ADP or ADP sensitivity are readily deaggregated.
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