Effects of oxyfedrin: a beta-adrenoreceptor stimulant, on infarct size following acute coronary artery ligation.

Abstract

Regional left ventricular blood flow and the extent of myocardial ischaemia were studied after acute coronary artery occlusion in open-chest dogs before and after infusion of oxyfedrin, a beta-adrenergic stimulant. Regional blood flow was measured with radioactive tracer microspheres and local tissue injury was estimated by the S-T segment elevation in epicardial electrocardiograms. Animals receiving oxyfedrin were divided into two groups: 1 and 2. Oxyfedrin was infused intravenously in a dose of 0.80 to 0.94 mg.kg-1 in dogs of group 1 and 1.45 to 1.60 mg.kg-1 in dogs of group 2. The rate of infusion in the animals of both groups was 0.61 mg.min-1. Oxyfedrin caused further S-T segment elevation over ischaemic myocardium and increased the extent of ischaemic injury in group 1 dogs. Conversely, in this same group of dogs, the blood flow was unchanged in low flow regions ( less than 0.3 cm3.g-1.min-1) and increased in higher flow areas, inside the ischaemic region. In the animals of group 2, oxyfedrin caused further S-T segment elevation over ischaemic myocardium and increased the extent of ischaemic injury. Concomitantly, blood flow was significantly reduced both inside and outside the ischaemic region. These observations in dogs of group 1 (ie increased blood flow inside the ischaemic region by infusion of oxyfedrin, in flow zones higher than 0.3 cm3.g-1.min-1, with a further S-T segment elevation over ischaemic myocardium, and an increase in the extent of ischaemic injury) may be explained by a primary effect of oxyfedrin on oxygen demands with secondary changes in blood flow.