Why the study?
Does aspirin ingestion affect lipid peroxidation recovery differently in heavy-large versus light-small human platelets?
Does aspirin ingestion affect lipid peroxidation recovery differently in heavy-large versus light-small human platelets?
The parallel recovery of lipid peroxidation in heavy and light platelets after aspirin ingestion challenges the hypothesis that platelet density and size are age-related.
Challenges age-density hypothesis for platelets in this animal model; leaves open relevance to human aspirin response and turnover.
Human platelets were separated into 2 density populations by repeated centrifugations of platelet-rich plasma at increasing gravitational force. The heaviest platelet fraction was rich in larger platelets. The lightest platelet fraction was rich in smaller platelets. In both fractions and in the platelet button, lipid peroxidation (malonaldehyde-MDA-production after addition of thrombin) was measured at basal condition, on the 1st, 3rd, 5th, 7th and 9th day after aspirin ingestion. At basal conditions and after ingestion of aspirin, MDA production was higher in the heavy-large platelets than in light-small ones, but a parallel increase of MDA production was observed in the light and in the heavy population and in the platelet button. The data are not compatible with the hypothesis that platelet density and size are age-related. Aspirin inhibits platelet lipid peroxidation by permanently acetylating their cyclooxygenase and if the heaviest platelets were the young ones, lipid peroxidation should reappear sooner in them.
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Leone et al. (1979) studied this question.
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