Transient effects of norepinephrine on myocardial oxygen balance.

In conscious dogs with experimental atrioventricular block and with ventricles paced at constant rate the effects of norepinephrine (NE) and isoproterenol (ISO) on coronary flow, coronary resistance, and myocardial O2-balance were investigated. Myocardial O2-S balance, as estimated from continuous measurement of coronary venous O2-S saturation, was used for the discrimination of coronary dilation induced either directly by vascular beta-adrenoreceptor stimulation or indirectly by increased myocardial metabolism. Following bolus injection of NE (0.3 microgram/kg) or ISO (0.1 microgram/kg) into the pulmonary artery, coronary venous O2-S saturation increased from a control of 25 +/- 2% O2-S saturation (mean +/- S.D.) transiently to 51 +/- 5 and 62 +/- 5% O2-S saturation respectively. After beta1-adrenoreceptor blockade these increases were reduced to 33 +/- 4 and 41 +/- 3% O2-S saturation, respectively. The remaining increase after NE was abolished when atropine was given in addition to beta1-b blockade. After beta1 + 2-adrenoreceptor blockade neither NE nor ISO injection had an effect on coronary venous O2 saturation. After beta1-b blockade was superimposed on ganglionic blockade NE injection led to a decrease in coronary venous O2-S saturation indicating a latent alpha-a activity of NE. NE seems to act directly via beta1-a adrenoreceptors, since no differences were observed in the time courses of changes in coronary venous O2-S saturation after left atrial injection of NE when compared to adenosine. It is concluded that circulating NE like ISO is able to improve myocardial oxygen balance by a direct vasodilating effect on canine coronary vessels mediated by vascular beta1-adrenoreceptors.