[Mechanism of action of oxyfedrine as a partial beta receptor agonist].

To investigate a possible dual action of oxyfedrine on beta-adrenergic receptors, hemodynamics and systolic time intervals were studied in 12 healthy volunteers during intravenous infusion of isoprenaline. The dose was titrated to a mean target heart rate of 113 bpm corresponding to an average dose of 6.16 micrograms/min. After return to baseline hemodynamics, oxyfedrine was administered as an intravenous bolus of 8 mg and the protocol was repeated. Compared to baseline, the percentage changes induced by isoprenaline at doses of 2.73 and 6.16 micrograms/min before and after (in parentheses) oxyfedrine were: heart rate: +33/+83% (+19/+62%); cardiac output: +90/153% (+30/+71%); systolic blood pressure: +16/+20% (+6/+7%); stroke volume: +42/+38% (+10/+6%); peripheral vascular resistance: -50/-63% (-31/-50%); cardiac work: +86/+148% (+19/+54%); pre-ejection period: -40/-56% (-27/-45%); isovolumic contraction time: -56/-79% (-29/-63%); systolic ejection rate: +67/+103% (+27/+52%); tension time index: +32/+50% (+7/+20%). Thus, the dose-dependent hemodynamic effects of isoprenaline were significantly attenuated by oxyfedrine pre-treatment with a shift of the dose-response curve to the right; this was attributed to a beta-antagonistic property of oxyfedrine. The results indicate that, in view of its well-known beta-stimulating effects, oxyfedrine exerts a dual action on adrenergic beta-receptors consistent with partial agonistic activity. Thereby, the different profiles of hemodynamic and metabolic actions of oxyfedrine compared to those of pure beta-agonistic agents can be explained as well as its beneficial therapeutic effects in patients with coronary heart disease.