Abstract
Canine hearts were perfused in vitro to investigate the role of norepinephrine on the temporary suppression of ventricular automaticity which follows fast drive rates (“overdrive suppression”). Norepinephrine administration (10 μg/L) increased the control rate and shortened the overdrive suppression at all rates of drive. When the rate of drive was kept constant and the concentration of norepinephrine varied, cycle length and overdrive suppression varied in a parallel manner with a maximal response usually between 10 to 20 μg/L norepinephrine concentration. When the pause durations were extrapolated at a selected percentage of overdrive, the pause duration was significantly shorter with norepinephrine. Pretreatment with reserpine led to an increase of overdrive suppression which was in excess of that expected from the slower control rate. Administration of norepinephrine restored the usual response. Beta receptor blockade with propranolol, while having little effect on the control rate, abolished the effect of noreprinephrine on overdrive suppression. It is concluded that norepinephrine decreases overdrive suppression with mechanisms which are in part unrelated to an increase in the control rate of discharge; that stored catecholamines counteract to some extent overdrive suppression; and that these adrenergic effects are mediated through a beta receptor mechanism.
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