Abstract
The EP effects of acute hypoxia (H) are probably responsible for many clinical arrhythmias (A) in children. Sotalol is a potent anti-A agent with classll (β-blocking) and ClassIII (Amiodarone-like) actions. Its D isomer (DS) should be devoid of β-blockade & be a pure ClassIII agent. We evaluated the cellular EP effects of DS on acutely hypoxic myocardium using rabbit atrial muscle and standard microelectrode techniques. Following control action potential (AP) recordings, tissues were exposed to 10−4M DS, acute H, or DS+H for 20 min. Continuous AP recordings showed no changes in maximum diastolic potential or Vmax from any intervention. The effects on AP amplitude (APA), AP duration (APD) at 50 and 90% repolarization and atrial effective refractory period (AERP) are shown (*p<0.05; +p<0.01):
By prolonging AERP and APD proportionally, DS showed typical ClassIII activity. Its acute onset and lack of antiadrenergic effects provide significant advantages over Amiodarone. DS does not, however, alter the EP effects of acute H and may be of little benefit in treating A induced or exacerbated by H.
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Yabek, S., Kato, R. & Singh, B. ELECTROPHYSIOLOGICAL (EP) EFFECTS OF D-SOTALOL ON HYPOXIG MYOCARDIUM. Pediatr Res 18 (Suppl 4), 133 (1984). https://doi.org/10.1203/00006450-198404001-00238
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DOI: https://doi.org/10.1203/00006450-198404001-00238