Effect of acetylsalicylic acid on experimentally induced arterial thrombosis in rats

Abstract

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.

High glucose contributes to aspirin insensitivity in streptozotocin-diabetic rats: a multiparametric aggregation study

“…The inhibition of platelet aggregation deepened with a higher dose of ASA, but it did not correspond to the increased occupation of free amino groups in platelet proteins, as the content of free amino groups was maintained at the same level for both low and high ASA doses. Noteworthy, in our study, only long-term administration of higher ASA doses lead to significant reductions in platelet aggregation and disaggregation, which is consistent with the outcomes reported earlier in experimental arterial thrombosis in rats by Meng and Seuter [34], who demonstrated that the duration of ASA action depended on the dose used, and even after a single high ASA dose the inhibitory effects of ASA on aggregation remained for several days. In our study, ASA was given continuously for 8 weeks, so we have no reason to doubt that such a cumulative drug effect remained permanent [52].…”

“…There are several reports on the use of ASA in rats, concerning its pharmacokinetics and antiplatelet action [33][34][35][36]. Platelet hypersensitivity and antiplatelet treatment with ASA in experimental diabetes in rats has been reported in earlier studies [36,37]; the effects of hyperglycaemia and protein glycation on the effectiveness of ASA therapy in diabetic animals have not so far been addressed.…”

Cerebrovascular Agents in Gerontopsychopharmacotherapy

“…These effects persisted for up to 2 days when the animals were given doses of 30 mg/kg orally (SEUTER, 1976). ASA also prevents venous as well as arterial thrombus formation in different animal species (MENG, 1975(MENG, , 1976SCHMIDT, 1975;MENG and SEUTER, 1977). Rabbits pretreated with ASA are protected against arachidonic-acid-induced thromboembolic death (SILVER et aI., 1974;SEUTER and BUSSE, 1979).…”

Cardiovascular Drugs

“…Finally, for the determination of an antithrombotic action, the vessel wall can be damaged by several means or an artificial arterioarterial or arterio-venous shunt is inserted and thrombus formation can be followed gravimetrically, by radioactive markers, histologically or by measuring the flow reduction [126][127][128][129][130][131]. [132] Thromboxane A 2 (TXA 2 ) is one of the most active mediators of aggregation (see Section 5.1).…”