Summary
Ethanol, at physiologically tolerable concentrations, did not affect the primary phase
of ADP-induced aggregation of human or rabbit platelets, which is not associated with
the secretion of granule contents. Potentiation by epinephrine of the primary phase
of ADP-induced aggregation of rabbit platelets was also not inhibited by ethanol.
However, ethanol did inhibit the secondary phase of ADP-induced aggregation which
occurs with human platelets in citrated platelet-rich plasma and is dependent on the
formation of thromboxane A2. Inhibition by ethanol of thromboxane production by stimulated platelets is likely
due to inhibition of the mobilization of arachidonic acid from membrane phospholipids,
as ethanol had little or no effect on aggregation and secretion induced by arachidonic
acid or the thromboxane mimetic U46619. Rabbit platelet aggregation and secretion
in response to low concentrations of collagen, thrombin, or PAF were inhibited by
ethanol. Inhibition of the effects of thrombin and PAF was also observed with aspirin-treated
platelets. Thus, in addition to inhibiting the mobilization of arachidonate for thromboxane
formation that occurs with most agonists, ethanol can also inhibit aggregation and
secretion through other effects on platelet responses.
Keywords
Platelet aggregation - Platelet secretion - Platelet inhibition - Ethanol
