ear if the residual differences in platelet function impact the drug's overall beneficial effects, and if the doses used in earlier studies were sufficient to decisively prevent heart attacks in women.
"Further research is required to get a definitive answer as to whom aspirin really benefits, under what circumstances it does work and does not work, and just how much is required in different people," he adds.
Results in both men and women showed that aspirin, taken daily for a two-week period, works by inhibiting key biological pathways that lead to platelet clumping.
Moreover, platelet aggregation was largely suppressed in at least three other key pathways related to their function when platelets were stimulated with substances that normally trigger clot formation. Each of these tests involved mixing whole blood, or platelet-rich plasma, from aspirin-treated men and women with various concentrations of each of the main chemical compounds involved in the pathways - collagen, adenosine diphosphate, and epinephrine - to see how platelets responded.
For example, in aspirin-treated men, platelet clumping went down by 14.6 ohms when 1 microgram of collagen per milliliter was added to whole blood, and decreased by 2.4 ohms when exposed to a higher dose of 5 micrograms per milliliter. In treated women, reductions were the same, at 14.9 ohms and 2.42 ohms, respectively.
When 10 micromoles per liter of adenosine diphosphate were added to whole blood, platelet aggregation decreased the same amount, 0.19 ohms in men and 0.21 ohms in women. Addition of 2 micromoles per liter of epinephrine to platelet-rich plasma produced significantly greater reductions in platelet clumping in treated women, a drop of 36.9 percent, while it was less of a reduction for men, at 31.5 percent. Again, the researchers say, these changes would have been zero if aspirin had had no effect.
Further analysis of results highlighted mainly two fac
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