Ephedra alkaloids inhibit platelet aggregation

Area of Science:

• Pharmacology
• Hematology
• Neuroscience

Background:

• Sympathomimetics, including Ephedra alkaloids, are linked to increased intracerebral hemorrhage, possibly due to elevated blood pressure.
• The precise mechanisms underlying this association, particularly effects on platelet function, require further investigation.

Purpose of the Study:

• To investigate the hypothesis that sympathomimetics decrease platelet aggregation.
• To determine the impact of common sympathomimetics on platelet function and intracellular signaling pathways.

Main Methods:

• Platelet-rich plasma from healthy individuals was used to measure aggregation responses to epinephrine in the presence of ephedrine, phenylpropanolamine, and racemic amphetamine.
• Intracellular cyclic AMP release and RANTES (regulated on activation, normal T cell expressed and secreted) were assayed ex vivo.
• Flow cytometry assessed platelet selectin (CD62p) activation, and data were analyzed using repeated-measures analyses of variance.

Main Results:

• Sympathomimetics significantly reduced epinephrine-mediated platelet aggregation.
• Ephedrine diminished aggregation responses to ADP and gamma-thrombin, and reduced RANTES exocytosis and basal CD62p expression.
• Caffeine potentiated ephedrine's effect on platelet function, while phenylpropanolamine amplified aspirin's inhibitory effect on aggregation.

Conclusions:

• Sympathomimetics markedly alter platelet function, potentially increasing bleeding risk independently of their hypertensive effects.
• Consumption of sympathomimetics should be considered in patients presenting with cerebral hemorrhage, even with existing restrictions on their use.