Platelet function studies in coronary artery disease. X. Effect of dipyridamole.
To evaluate the effects of dipyridamole on blood platelet function in patients with coronary artery disease, platelet counts and aggregation were examined in aortic and coronary venous blood. Before administration of dipyridamole, platelet counts and aggregation in response to adenosine diphosphate were less (p less than 0.02) in coronary venous than in aortic blood. Dipyridamole administration (100 mg) resulted in an increase in platelet counts and platelet aggregation in coronary venous blood so that the differences in aortic and coronary venous blood values were eliminated. These phenomena were probably related to inhibitory actions of dipyridamole on platelet adhesion to atherosclerotic vessels. To further study the mechanism of action, the direct effects of dipyridamole on in vitro platelet aggregation were evaluated. Although dipyridamole, in the concentrations used, had no effect on in vitro platelet aggregation, it greatly potentiated the aggregation inhibitory actions of exogenous prostacyclin. In vivo potentiation of endogenous prostacyclin and inhibitory actions on platelet adhesion are the most likely mechanisms of the potentially beneficial actions of dipyridamole.
D000244:Adenosine Diphosphate; D000328:Adult; D001792:Blood Platelets / Q000187:drug effects*; D003327:Coronary Disease / Q000097:blood* / Q000188:drug therapy; D004176:Dipyridamole / Q000627:therapeutic use*; D004357:Drug Synergism; D011464:Epoprostenol / Q000494:pharmacology; D006801:Humans; D008875:Middle Aged; D010973:Platelet Adhesiveness / Q000187:drug effects; D010974:Platelet Aggregation / Q000187:drug effects; D010976:Platelet Count
D000244:Adenosine Diphosphate; D004176:Dipyridamole; D011464:Epoprostenol