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The inotropic effects of norepinephrine are attributed to increase in myocardial contractility and decrease in adrenergic receptor sensitivity. However, this hypothesis has been challenged by lack of reproducible inotropic effects with increased beta-adrenergic stimulation. The purpose of this study was to evaluate ventricular tachycardia induction during norepinephrine-induced stress with isolated perfused hearts. Left ventricular function was measured with a balloon tip catheter, and monophasic action potentials from the septum and posterior right ventricular wall were recorded. Conventional end points were used to differentiate between acute local toxicity and inotropic action of norepinephrine. Hearts from 10 anesthetized mongrel dogs were perfused according to Langendorff technique. Coronary perfusion pressure was monitored, and norepinephrine was infused to obtain an increase in coronary perfusion pressure. Each heart was exposed to 10 infusions of norepinephrine at 10, 20, 40, and 80 micrograms/min. Ventricular tachycardia was induced in one of 12 hearts at norepinephrine 20 micrograms/min or 40 micrograms/min, whereas tachycardia was never induced at the 10-micrograms/min norepinephrine infusion. Norepinephrine 40 and 80 micrograms/min infusion resulted
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