Arterial and venous tissues from normal rats generate a potent inhibitor of platelet aggregation with the characteristics of prostacyclin (PGI2). Vascular tissues from rats made moderately or severely thrombocytopenic (by administration of heterologous antiplatelet antiserum) release prostacyclin-activity in the same way as the corresponding vessels from normal rats. This activity was inhibited by administration of acetylsalicylate to both normal and thrombocytopenic rats. It is suggested that the basal release of prostacyclin from rat vasculature is independent of the number of circulating platelets and that rat vessels possess both the substrates and the enzymes required for prostacyclin generation. The possibility that chronic thrombocytopenia might affect prostacyclin generation by inducing endothelial damage, cannot be excluded.
ASJC Scopus subject areas
- Cardiology and Cardiovascular Medicine