Intravenous aspirin at reperfusion does not reduce infarct size in the dogwith a residual critical stenosis

Platelet-related events being associated with the increment of infarct size at reperfusion in the presence of a residual stenosis, we tested in dogs w hether intravenous aspirin (ASA) could limit infarct size. The left anterio r descending coronary artery was occluded for 90 min and reperfused for 6 h in the presence of a residual critical stenosis. Controls received saline, and treated groups were given 2, 6, or 12 mg/kg ASA, i.v., 5 min before re perfusion. Infarct size did not differ significantly between groups (contro l, 43.80 +/- 6.28%; ASA, 2 mg/kg: 41.07 +/- 7.78%; ASA, 6 mg/kg: 37.55 +/- 3.44%; ASA, 12 mg/kg: 29.40 +/- 5.41%), as well as transmural collateral bl ood flow and [In-111]-platelet accumulation in the infarcted myocardium (2. 5-3.6 x 10(5) platelets/g). However, myocardial neutrophil accumulation was significantly reduced (p < 0.05) in groups given 6 (15.0 +/- 2.6 x 10(6)/g tissue) and 12 mg/kg (18.4 +/- 3.8) ASA, but not in the 2-mg/kg group (21. 0 +/- 5.2), as compared with control group (32.0 +/- 7.2). Ex vivo platelet aggregation to collagen was abolished during reperfusion in all treated gr oups (p < 0.05), Transcardiac arteriovenous differences in 6-keto-PGF(1 alp ha) were reduced significantly 1 h after reperfusion in groups given 6 or 1 2 mg/kg ASA (94.7 +/- 13.1 and 71.7 +/- 19.2 pg/ml, respectively) but not i n the 2-mg/kg group (178.3 +/- 78.2 pg/ml), as compared with control (405.4 +/- 171.6 pg/ml). ASA-insensitive platelet activation at the site of steno sis or inhibition by ASA of prostacyclin production by jeopardized myocardi um may explain the observed lack of benefit of ASA.