Key result
Dipyridamole inhibited platelet aggregation and adhesiveness in vitro and showed a trend toward lessening ADP-induced clumping when administered orally at 100 mg 4 times daily.
Why the study?
Does dipyridamole inhibit platelet aggregation and adhesiveness in human plasma and whole blood?
Does dipyridamole inhibit platelet aggregation and adhesiveness in human plasma and whole blood?
Dipyridamole demonstrates antiplatelet effects by inhibiting aggregation and adhesiveness, suggesting potential utility in arterial disease.
Answers are grounded in this paper and cite their sources.
In vitro antiplatelet effects in animals leave open human efficacy for arterial disease; prospective trials required.
The effect of dipyridamole (Persantin) on platelet behaviour in human plasma and whole blood has been studied in three experimental systems. Added to plasma and whole blood in a concentration of 50 μg. per ml., dipyridamole inhibited platelet aggregation in a Chandler tube system, and ADP-induced clumping in a turbidimetric system. Adhesiveness of platelets to glass beads in a Hellem system was also decreased by the drug. Oral administration in doses of 100 mg. 4 times per day suggests a trend in which ADP-induced clumping is lessened after therapy with the drug and one patient is recorded in whom a reduction in platelet adhesiveness to glass beads can probably be attributed to the drug. The results of this trial coupled with those of previous workers suggest that clinical trials of dipyridamole in human arterial disease are indicated to define the place of this drug in the therapy of arterial disease.
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Gray et al. (1968) studied this question. Dipyridamole was evaluated on Platelet aggregation and adhesiveness. Dipyridamole inhibited platelet aggregation and adhesiveness in vitro and showed a trend toward lessening ADP-induced clumping when administered orally at 100 mg 4 times daily.
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