Key result
In vitro cocaine treatment modified rabbit platelet responsiveness, increasing aggregation and thromboxane production at low concentrations while inhibiting prostacyclin release from aortic tissue.
Why the study?
Does in vitro cocaine treatment alter platelet responsiveness, thromboxane production, and prostacyclin synthesis in rabbit platelet-rich plasma and aortic tissue?
Population
Rabbit platelet-rich plasma and aortic tissue (in vitro model)
Design
Preclinical
Authors
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Cocaine may enhance platelet reactivity in vitro; leaves open relevance to thrombotic risk in users.
Does in vitro cocaine treatment alter platelet responsiveness, thromboxane production, and prostacyclin synthesis in rabbit platelet-rich plasma and aortic tissue?
In vitro cocaine treatment alters platelet aggregation and eicosanoid synthesis in rabbit models, likely by modifying calcium membrane binding and influx.
Togna et al. (2009) studied this question. Cocaine hydrochloride was evaluated on Platelet responsiveness to arachidonic acid, thromboxane production, and prostacyclin release. In vitro cocaine treatment modified rabbit platelet responsiveness, increasing aggregation and thromboxane production at low concentrations while inhibiting prostacyclin release from aortic tissue.
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