Aspirin (acetylsalicylic acid) has inhibitory effects on platelet function and prostaglandin synthesis. Since alterations in either platelet function or prostaglandin-mediated vascular responses could influence blood flow to ischemic myocardium, we tested the effects of aspirin on coronary collateral flow after acute occlusion of the left anterior descending coronary artery in dogs. Aspirin dose (600 mg i.v.) consistently inhibited in vitro ADP-induced platelet aggregation. In 13 open-chest dogs, regional myocardial blood flows (radioactive microsphere technique) were determined at 5 minutes and 4 hours after occlusion. In seven of these Jogs, aspirin (600 mg i.v.) was administered I hour before occlusion. In the aspirin-treated dogs, collateral rn';w increased significantly (p>0.05), from 0.09 ± 0.02 ml/min/g at 5 minutes to 0.15 and 0.02 ml/min/g 4 μrs after occlusion. Collateral flow was not significantly altered over 4 hours in control dogs. The aspirin-)lJuced increase in collateral flow was confined to epicardium (12 ± 4% of normal zone flow at 5 minutes to 4% at 4 hours after occlusion).