Key result
Isoprenaline doubles net frequency-dependent myocardial potassium flux ~2-fold during pacing changes.
Why the study?
The frequency dependent myocardial potassium fluxes of intact pig hearts at control inotropy and during beta adrenergic stimulation needed to be determined.
Does beta-adrenergic stimulation with isoprenaline increase frequency-dependent myocardial potassium fluxes in intact pig hearts?
Does beta-adrenergic stimulation with isoprenaline increase frequency-dependent myocardial potassium fluxes in intact pig hearts?
In intact pig hearts, beta-adrenergic stimulation with isoprenaline doubles the frequency-dependent myocardial potassium flux, accounting for 22-25% of the ouabain-inhibitable potassium flux.
Answers are grounded in this paper and cite their sources.
No immediate clinical implications; leaves open translation of beta-adrenergic effects on myocardial potassium handling to human arrhythmia risk.
Study objective The aim was to determine the frequency dependent myocardial potassium fluxes of intact pig hearts at control inotropy and during beta adrenergic stimulation. DESIGN - Atrial pacing rate was suddenly raised and decreased by 50 beats.min-1 at control inotropy and during infusion of isoprenaline, 2.5 nmol.min-1, into the left coronary artery. Experimental material Nine anaesthetised pigs (21-33 kg) were instrumented for electric pacing of the right atrium and metabolic and haemodynamic recordings. Measurements and main results Myocardial potassium balance was measured by PVC-valinomycin electrodes in the left atrial cavity and in a shunt (with flow meter) diverting blood from the coronary sinus to the right atrium. Isoprenaline raised net myocardial potassium flux following the change in pacing rate from 19(14-23) to 38(32-46) mumol.100 g-1.min-1 (median, 95% confidence interval, difference: p = 0.03). The corresponding myocardial potassium flux per beat increased from 0.38(0.29-0.45) to 0.80(0.63-0.97) mumol.100 g-1 (p = 0.03). Accumulated potassium flux increased from 9(8-11) to 17(11-27) mumol.100 g-1, respectively (p = 0.03). Conclusions In intact hearts beta adrenergic stimulation doubles the frequency dependent myocardial potassium flux. This component constitutes 22-25% of the ouabain inhibitable potassium flux at both levels of inotropy.
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Ellingsen et al. (1991) studied Frequency dependent myocardial potassium fluxes (n=9). Isoprenaline infusion during sudden atrial pacing rate changes (±50 beats·min-1) vs. Control inotropy during sudden atrial pacing rate changes (±50 beats·min-1) was evaluated on Net myocardial potassium flux following pacing rate change (mumol·100 g-1·min-1) (p=0.03). Isoprenaline infusion doubled net frequency-dependent myocardial potassium flux from 19 (95% CI 14-23) to 38 (95% CI 32-46) mumol·100 g-1·min-1 (p=0.03).
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