Thromb Haemost 1988; 59(03): 383-387
DOI: 10.1055/s-0038-1647500
Original Article
Schattauer GmbH Stuttgart

Effects of Ethanol on Pathways of Platelet Aggregation In Vitro

Margaret L Rand
The Department of Biochemistry, University of Toronto, Toronto, Canada and the Department of Pathology, McMaster University, Hamilton, Canada
,
Marian A Packham
The Department of Biochemistry, University of Toronto, Toronto, Canada and the Department of Pathology, McMaster University, Hamilton, Canada
,
Raelene L Kinlough-Rathbone
The Department of Biochemistry, University of Toronto, Toronto, Canada and the Department of Pathology, McMaster University, Hamilton, Canada
,
J Fraser Mustard
The Department of Biochemistry, University of Toronto, Toronto, Canada and the Department of Pathology, McMaster University, Hamilton, Canada
› Author Affiliations
Further Information

Publication History

Received 24 August 1987

Accepted after revision 11 January 1988

Publication Date:
29 June 2018 (online)

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.

 
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