BACKGROUND: The electrophysiologic effects of norepinephrine (NE) in human beings have not been previously described. METHODS: The electrophysiologic effects of NE infused at a rate of 25 ng/kg/min were determined in 21 patients with a mean age of 41 +/- 11 years and without structural heart disease who underwent an electrophysiology procedure. In a subgroup of 10 patients electrophysiologic parameters were measured at baseline, after the infusion of NE, and after administration of beta-blockade while in continuous NE infusion. RESULTS: The baseline NE plasma concentration of 298 +/- 153 pg/ml increased to 708 +/- 419 pg/ml after the infusion of NE. NE significantly increased the mean blood pressure, sinus cycle length, corrected sinus node recovery time, ventriculoatrial block cycle length, and the atrial and ventricular effective refractory periods. In a subset of 10 patients 0.2 mg/kg propranolol administered during continued infusion of NE resulted in a further increase in sinus cycle length, atrial-His interval, and ventricular refractoriness. CONCLUSION: A physiologic elevation in the plasma NE concentration results in a depression of sinus node function and atrioventricular conduction and in prolongation of atrial and ventricular refractoriness. Some of NE's effects are partially offset by beta-adrenergic stimulation.
BACKGROUND: The electrophysiologic effects of norepinephrine (NE) in human beings have not been previously described. METHODS: The electrophysiologic effects of NE infused at a rate of 25 ng/kg/min were determined in 21 patients with a mean age of 41 +/- 11 years and without structural heart disease who underwent an electrophysiology procedure. In a subgroup of 10 patients electrophysiologic parameters were measured at baseline, after the infusion of NE, and after administration of beta-blockade while in continuous NE infusion. RESULTS: The baseline NE plasma concentration of 298 +/- 153 pg/ml increased to 708 +/- 419 pg/ml after the infusion of NE. NE significantly increased the mean blood pressure, sinus cycle length, corrected sinus node recovery time, ventriculoatrial block cycle length, and the atrial and ventricular effective refractory periods. In a subset of 10 patients 0.2 mg/kg propranolol administered during continued infusion of NE resulted in a further increase in sinus cycle length, atrial-His interval, and ventricular refractoriness. CONCLUSION: A physiologic elevation in the plasma NE concentration results in a depression of sinus node function and atrioventricular conduction and in prolongation of atrial and ventricular refractoriness. Some of NE's effects are partially offset by beta-adrenergic stimulation.