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Research Article Free access | 10.1172/JCI105903

The effect of salicylates on the hemostatic properties of platelets in man

Harvey J. Weiss, Louis M. Aledort, and Shaul Kochwa

Department of Medicine (Hematology), The Mount Sinai Hospital and School of Medicine of the City University of New York, New York 10029

The City Hospital at Elmhurst, New York 11373

Find articles by Weiss, H. in: PubMed | Google Scholar

Department of Medicine (Hematology), The Mount Sinai Hospital and School of Medicine of the City University of New York, New York 10029

The City Hospital at Elmhurst, New York 11373

Find articles by Aledort, L. in: PubMed | Google Scholar

Department of Medicine (Hematology), The Mount Sinai Hospital and School of Medicine of the City University of New York, New York 10029

The City Hospital at Elmhurst, New York 11373

Find articles by Kochwa, S. in: PubMed | Google Scholar

Published September 1, 1968 - More info

Published in Volume 47, Issue 9 on September 1, 1968
J Clin Invest. 1968;47(9):2169–2180. https://doi.org/10.1172/JCI105903.
© 1968 The American Society for Clinical Investigation
Published September 1, 1968 - Version history
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Abstract

Ingestion of 1.5 g of aspirin, but not of sodium salicylate, produced a significant prolongation of the bleeding time in six normal male subjects when compared with the effects of a placebo. Similar differences in the effect of the two drugs on platelets was also observed. Aspirin ingestion resulted in impaired platelet aggregation by connective tissue and was associated with a decreased release of platelet adenosine diphosphate (ADP); sodium salicylate had no effect on these values. In vitro, incubation of platelet-rich plasma with an optimum aspirin concentration of 0.50 mmole/liter (0.045 mg/ml) inhibited both the adhesion of platelets to connective tissue and the release of ADP as well as the secondary wave of platelet aggregation produced with ADP or epinephrine; sodium salicylate had no effect on these reactions, which were also normal in patients with von Willebrand's disease. The inhibitory effect produced by ingesting a single 1.8 g dose of aspirin was detectable for 4-7 days at which time salicylate was no longer detectable in the blood, which suggested an irreversible effect on the platelet. Aspirin also inhibited the release of platelet adenosine triphosphate (ATP), but had no effect on the platelet surface charge, available platelet ATP or ADP, or the destruction of ADP by plasma ADPase. These studies lend further support to the hypothesis that ingestion of aspirin, in contrast to sodium salicylate, prolongs the bleeding time by inhibiting the release of platelet ADP, perhaps reflecting the findings in other cell systems which suggest that aspirin alters membrane permeability.

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