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Thromb Haemost 1973; 30(03): 577-585
DOI: 10.1055/s-0038-1649136
Original Article
Schattauer GmbH

Effect of Aspirin and Benadryl on Human Platelet Oxidative Phosphorylation and Aggregation

Kenneth T. N. Yue
1   Hematology Research Laboratory, Veterans Administration Hospital, Kansas City, Missouri 64128
2   Departments of Pathology and Medicine, University of Kansas School of Medicine, Kansas City, Kansas 66103
,
James W. Davis
1   Hematology Research Laboratory, Veterans Administration Hospital, Kansas City, Missouri 64128
2   Departments of Pathology and Medicine, University of Kansas School of Medicine, Kansas City, Kansas 66103
,
E. Gray Aldridge
1   Hematology Research Laboratory, Veterans Administration Hospital, Kansas City, Missouri 64128
2   Departments of Pathology and Medicine, University of Kansas School of Medicine, Kansas City, Kansas 66103
› Author Affiliations
Further Information

Publication History

Received 20 April 1973

Accepted 14 August 1973

Publication Date:
30 June 2018 (online)

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Summary

Tightly coupled oxidative phosphorylation in washed human platelets and in lysates has been demonstrated. Both aspirin (25 μM) and Benadryl (0.15 mM) inhibited phosphorylating oxidation but had no effect on uncoupled respiration. It is likely that they were not involved in the electron transport chain but specifically affected the phosphorylation reactions similar to the action of oligomycin. Preincubation of Benadryl (1.3 mM) with platelet-rich plasma (PRP) at room temperature for 2 min inhibited ADP-induced platelet aggregation by 62% and abolished the second phase of aggregation. Addition of Benadryl to aggregating platelets in PRP during ADP-induced aggregation caused immediate disaggregation whether added during the first or second phase of aggregation. Aspirin had no such effect.

 

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