Effects on platelet aggregation were examined of acetylsalicylic acid (ASA), indomethacin and a number of other agents including dipyridamole, phenylbutazone and sulfinpyrazone under standardized conditions. The Born turbidometric method of measuring platelet aggregation was used with collagen as the stimulus for aggregation. ASA and indomethacin were shown to be among the most potent inhibitors of aggregation, being active at minimal effective concentrations of 1–3 μg/ml using a 10 min time of pre-incubation with the platelet-rich plasma (degree of aggregation inhibition was time dependent). Most of the other agents tested were also active in vitro and both prostaglandin El and adenosine were more potent than ASA or indomethacin. However, these agents were shown not to exert significant inhibitory effects when administered orally to rats (dose 10 and 30 mg/kg). ASA proved to be effective in doses as low as 3 mg/kg, and indomethacin in doses as low as 1 mg/kg orally. The inhibitory effects of ASA on aggregation remained for several days after a single oral dose, whereas the effects of indomethacin disappeared within 24 h.

Acetylsalicylic acid (ASA) was tested for its antithrombotic activity in the arterial system after prophylactic administration to rats, using a new standardized method. Damage of the vessel wall was produced by chilling a small segment of the left carotid artery. Dose related, significant results were obtained after 3 mg/kg orally. If higher doses (10 and 30 mg/kg) are administered, the formation of non-occlusive thrombi is inhibited by 70--90% on the basis of thrombus weight. As the frequency distributions show, there are significantly more zero-values in the ASA treated groups (total 50%) than in the control groups. However, the incidence of occlusive thrombi was not changed by ASA. The long-lasting effect of ASA in inhibition of platelet aggregation was confirmed. The formation of arterial thrombi is significantly inhibited after prophylactic administration of 30 and 10 mg/kg up to 48 h before initiation of thrombosis. After administration of 3 mg/kg orally, only insignificant effects were observed. Thus the duration of action depends on the dose used.

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