The effect of delay in propranolol administration on reduction of myocardial infarct size after experimental coronary artery occlusion in dogs.

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Abstract
The effects of i.v. propranolol (2 mg/kg) on myocardial ischemic injury in relation to the influence of delay in therapy on gross infarct size (GIS) were determined in 39 closed-chest anesthetized dogs in which the left anterior descending coronary artery (LAD) was occluded at a fixed distance from its origin by a balloon catheter. Precordial ECG maps, hemodynamic variables and serum CK [creatine kinase] levels were monitored for 24 h. After 24 h, GIS were estimated from the measured areas of ischemic discoloration in serial sections of the left ventricle (LV). In 9 dogs, propranolol administration was started before LAD occlusion, in another 9, 3 h and in 10 others, 6 h after occlusion; the remainder (n = 11) served as controls. In the dogs pretreated with propranolol, the GIS (14.0 .+-. 4.0 g or 10.0 .+-. 2.0% of LV [left ventricular] wt) was 53% smaller (P < 0.01) than in the controls (29.0 .+-. 2.0 g or 22.0 .+-. 1.0% of LV wt); those given propranolol 3 h after occlusion had 28% smaller (P < 0.05) GIS (19.0 .+-. 2.0 g or 15.0 .+-. 2.0% LV wt) than the controls. GIS in the dogs receiving propranolol 6 h after occlusion (24.0 .+-. 3.0 g or 19.0 .+-. 3.0% of LV wt) was not significantly different from that in the controls. The beneficial effect of propranolol on GIS was accompanied by corresponding directional changes in the precordial ST-segment elevation and in the rate of decline of the R-wave amplitude of the ECG. Propranolol reduced the heart rate and cardiac output for 5-6 h in pretreated dogs; in dogs given propranolol 3 and 6 h after occlusion, heart rate was reduced for 3-4 h, but cardiac output remained low for the remainder of the 24 h. The beneficial effect of propranolol on GIS varies inversely with the delay in drug administration after LAD occlusion and no effect is apparent when propranolol infusion is begun 6 h after occlusion.