Abstract
Aspirin produces alteration of platelet function characterized by loss of secondary aggregation in response to ADP or epinephrine, and inhibition of aggregation by collagen. In addition, platelet factor 3 release by these reagents is reduced. A similar platelet lesion was produced by an acetylating agent, acetic anhydride, supporting earlier concepts that aspirin activity against platelets may be a consequence of acetylation. An attempt to identify specific acetylation of platelets with acetyl-1-14C salicylic acid was unsuccessful. Although platelet uptake of the label was demonstrated, metabolic incorporation of acetate could not be excluded.
Original language | English (US) |
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Pages (from-to) | 632-636 |
Number of pages | 5 |
Journal | Proceedings of the Society for Experimental Biology and Medicine |
Volume | 133 |
Issue number | 2 |
DOIs | |
State | Published - Feb 1970 |
All Science Journal Classification (ASJC) codes
- General Biochemistry, Genetics and Molecular Biology