Trial of repeated low-dose aspirin in diabetic angiopathy.
We compared the ability of aspirin to suppress platelet aggregation and thromboxane synthesis in ten normal subjects and ten patients with diabetic angiopathy and high rate of entry of new platelets into the circulation. When single doses of 100 to 1,000 mg aspirin were ingested daily for 1 month, there were time gaps between doses in which platelets from diabetics and normals aggregated and formed thromboxane ex vivo in response to the combination of arachidonic acid plus collagen. Similar gaps were also found for diabetics, but not for normals, following four daily doses (every six hours) of 25 or 100 mg. Our data show that dose schedules of aspirin which may suffice in normals are not effective in patients with diabetic angiopathy, presumably because these patients have a high rate of entry of new platelets into the circulation. We suggest that continual suppression of platelet thromboxane synthesis and aggregation by low-dose, "slow-release" preparations of aspirin would be an ideal long-term approach for the prevention of thrombosis in patients with a high rate of entry of new platelets into the circulation.
D000255:Adenosine Triphosphate / Q000378:metabolism; D000328:Adult; D016718:Arachidonic Acid; D001095:Arachidonic Acids / Q000494:pharmacology; D001241:Aspirin / Q000008:administration & dosage*; D001792:Blood Platelets / Q000502:physiology*; D003094:Collagen / Q000494:pharmacology; D003920:Diabetes Mellitus / Q000188:drug therapy*; D003925:Diabetic Angiopathies / Q000188:drug therapy*; D004334:Drug Administration Schedule; D005260:Female; D006801:Humans; D008297:Male; D008315:Malondialdehyde / Q000097:blood; D008875:Middle Aged; D010974:Platelet Aggregation; D013929:Thromboxane B2 / Q000096:biosynthesis
D001095:Arachidonic Acids; D016718:Arachidonic Acid; D008315:Malondialdehyde; D013929:Thromboxane B2; D000255:Adenosine Triphosphate; D003094:Collagen; D001241:Aspirin