Platelet survival (PS) may be decreased in some thromboembolic disorders. Treatment of patients with drugs that suppress platelet function may or may not be associated with normalisation of PS. It is uncertain, however, whether a lack of influence on PS necessarily indicates lack of an antithrombotic effect. We have examined this problem in an arterial thrombosis model in rabbits. A non-occlusive mural thrombus was produced in the aortic arch and PS studied using 51Cr-labelled homologous platelets. Thrombus size was assessed by measuring 51Cr accretion. Three groups of 15 animals were studied as follows:group A - thrombus induced 30 min prior to start of PS, group B- as for group A but animals treated with SUL (25 mg/Kg) and ASA (25 mg/Kg) prior to thrombus induction and 12 hrly thereafter and group C- sham operated controls. Animals in group B showed a 45% reduction in thrombus size when compared with group A (p<0.05). The platelet Tl/2 in groups A, B, and C were 25.7, 25.6, and 33.8 hrs respectively. The difference between groups A and C and between groups B and C was significant (p<0.01).Thus, treatment with SUL and ASA reduced thrombus size but did not modify the change in PS associated with thrombus induction. Re-examination of PS data by 7 different analytical methods established that all were equally sensitive in discriminating thrombosis but all failed to detect a drug effect. It is concluded that failure to modify platelet survival does not necessarily exclude an antithrombotic effect and that this apparent lack of sensitivity does not relate to the method of data analysis used.