Impaired interaction (adhesion-aggregation) of platelets with the subendothelium in storage-pool disease and after aspirin ingestion. A comparison with von Willebrand's disease.
Possible defects in the interaction of platelets with the subendothelial surface were evaluated in six patients with storeage-pool disease, nine patients with von Willebrand's disease and seven normal subjects who ingested aspirin. Citrated blood was perfused through a chamber containing everted segments of rabbit aorta previously denuded of endothelium by means of a ballon catheter. With normal blood, 83.3 +/- 1.9 per cent (S.E.M.) of the surface was covered by adherent platelets. Platelet adhesion was normal after aspirin ingestion (89.7 +/- 4.6 per cent) and decreased in some patients with storage-pool disease. The most striking defect in both circumstances was the virtual absence of platelet thrombi. In contrast, decreased adhesion (57.3 +/- 3.4 per cent), but normal thrombus formation, was characteristic of von Willebrand's disease. These types of defects in platelet adhesion and aggregation may account for the hemostatic defects in a variety of bleeding disorders. The findings further suggest the possible usefulness of aspirin as an antithrombotic agent.
D000244:Adenosine Diphosphate / Q000378:metabolism*; D000284:Administration, Oral; D000293:Adolescent; D000328:Adult; D000818:Animals; D001012:Aorta, Abdominal; D001241:Aspirin / Q000008:administration & dosage / Q000494:pharmacology*; D001791:Blood Platelet Disorders / Q000097:blood*; D001792:Blood Platelets / Q000648:ultrastructure; D004727:Endothelium; D006801:Humans; D066298:In Vitro Techniques; D008875:Middle Aged; D010973:Platelet Adhesiveness / Q000187:drug effects; D010974:Platelet Aggregation / Q000187:drug effects; D011696:Purpura, Thrombocytopenic / Q000097:blood; D011817:Rabbits; D013577:Syndrome; D014842:von Willebrand Diseases / Q000097:blood*
D000244:Adenosine Diphosphate; D001241:Aspirin