Key result
Beta-blockers depress isoprenaline-induced ventricular automaticity, potentially impairing beta-mimetic response during resuscitation.
Why the study?
The role of beta-adrenergic receptors in controlling cardiac automaticity and the impact of beta-receptor blocking drugs on isoprenaline-induced idioventricular rhythm in man were not fully understood.
Do beta-receptor blocking agents depress isoprenaline-induced idioventricular rhythm in patients with Stokes-Adams disease?
Do beta-receptor blocking agents depress isoprenaline-induced idioventricular rhythm in patients with Stokes-Adams disease?
Beta-blockers depress isoprenaline-induced ventricular automaticity, potentially reducing the efficacy of beta-mimetics during emergency resuscitation for ventricular standstill.
May blunt isoprenaline response in ventricular standstill; leaves open clinical relevance for resuscitation in Stokes-Adams disease.
AbstractA method for studying drug effects on cardiac automaticity in man is presented. During the treatment for Stokes‐Adams disease emergency resuscitation from ventricular standstill can be effected by the arousal of intrinsic ventricular pacemakers. Isoprenaline seems to be a useful drug to produce idioventricular rhythm, but as shown in the present investigation its effect varies widely from patient to patient. The isoprenaline‐induced increase in the ventricular automaticity was depressed by the beta‐receptor blocking compounds propranolol and INPEA. The compounds seemed to block this effect of isoprenaline more easily than the effect of isoprenaline on the sino‐atrial rate. The observations indicate that adrenergic beta‐receptors are significantly involved in the control of cardiac automaticity in man. The observed effects of the beta‐receptor blocking drugs have an important clinical implication. In patients treated with the drugs the efficiency of beta‐mimetic substances in emergency resuscitation from ventricular standstill may be critically reduced.
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Michaeli et al. (1968) studied Stokes-Adams disease. Beta-receptor blocking compounds (propranolol and INPEA) was evaluated on Isoprenaline-induced increase in ventricular automaticity. Beta-receptor blocking compounds (propranolol and INPEA) depressed isoprenaline-induced increases in ventricular automaticity, potentially reducing beta-mimetic efficacy in emergency resuscitation.
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