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Slowing Na+ Channel Inactivation Prolongs QT Interval and Aggravates Adrenaline-Induced Arrhythmias
[摘要] References(25)Cited-By(6)We investigated the effects of prolonged repolarization induced by slowed inactivation of Na+ channel on adrenaline-induced arrhythmias in halothane anesthetized, closed-chest dogs. We used sea anemone toxins (ATX-II and Anthopleurin-A) to prolong ventricular repolarization and examined their effects on adrenaline arrhythmias. Sea anemone toxins prolonged the QTc- and JTc-intervals (P+ channels by class III drugs, which we have already reported, slowing Na+ channel inactivation with QTc prolongation also aggravates adrenaline-induced arrhythmias.
[发布日期]  [发布机构] 
[效力级别]  [学科分类] 药理学
[关键词] Adrenergic;ECG;long QT syndrome;Na+ channel;Ventricular arrhythmia [时效性] 
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