Cardiovasc Res. 1990 May;24(5):404-10. doi: 10.1093/cvr/24.5.404.
Attenuation of the rise in extracellular potassium concentration during myocardial ischaemia by d.l-sotalol and d-sotalol.
Cardiovascular research
M N Hicks, S M Cobbe
Affiliations
Affiliations
- Department of Medical Cardiology, Royal Infirmary, Glasgow, United Kingdom.
PMID: 2372795
DOI: 10.1093/cvr/24.5.404
Abstract
STUDY OBJECTIVE: The aim was to study the effects of d.l-sotalol, d-sotalol or atenolol on the rate of rise of extracellular potassium concentration [( K+]o) and the electrophysiological changes that occur during myocardial ischaemia.
DESIGN: The study was performed in isolated, arterially perfused interventricular septa from rabbit. Six septa were treated with d.l-sotalol 10(-4) mol.litre-1, six with d-sotalol 10(-4) mol.litre-1, six with atenolol 10(-5) mol.litre-1, and there were seven untreated controls. At these concentrations d.l and d-sotalol are equipotent in their class III effect, though d-sotalol has only 7% of the beta blocking activity of the racemic form, and atenolol is equipotent in its beta blocking activity to d.l-sotalol. [K+]o and electrophysiological variables were compared before and during a 30 min period of global zero flow ischaemia.
MEASUREMENTS AND MAIN RESULTS: Prior to ischaemia [K+]o, measured using potassium sensitive valinomycin electrodes, was similar in all the groups. [K+]o rose during ischaemia in all the groups, and at 30 min was 13.0 (SEM 0.7) mmol.litre-1 in the control group which was not different from 12.7(0.5) mmol.litre-1 in the atenolol group. In the d.l and d-sotalol groups the increases were markedly attenuated, reaching 9.2(1.0) and 8.8(0.7) mmol.litre-1 respectively. During ischaemia the class III effect of d.l and d-sotalol was lost within 6 min though the fall in maximum upstroke velocity of the action potentials (dV/dtmax) and the extent of resting membrane potential (Em) depolarisation were less in comparison to the control and atenolol groups.
CONCLUSIONS: The results indicate an attenuation by sotalol of the ischaemic rise in [K+]o, with preservation of dV/dtmax and Em, despite the loss of an effect on action potential duration. This potentially antiarrhythmic effect of sotalol in ischaemic myocardium is attributable to a direct membrane effect rather than beta adrenoceptor antagonism.
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