Key result
In isolated rat ventricular myocytes, the cardiac glycoside digitoxin increased arrhythmogenic spontaneous Ca(2+) waves and RyR2 oxidation, effects prevented by antioxidants and specific inhibitors.
Why the study?
Does digitoxin induce arrhythmogenesis through ROS-mediated redox modification of ryanodine receptors in isolated rat ventricular myocytes?
Does digitoxin induce arrhythmogenesis through ROS-mediated redox modification of ryanodine receptors in isolated rat ventricular myocytes?
The arrhythmogenic toxicity of cardiac glycosides is mediated by ROS-dependent oxidation of ryanodine receptors, highlighting a novel mechanism beyond Na+/K+-ATPase inhibition.
No takes yet. Share an insight, caveat, or question.
May implicate ROS-RyR oxidation in digitoxin arrhythmogenicity in rat myocytes; hypothesis-generating and requires in vivo/human validation before clinical relevance.
Ho et al. (2011) studied Arrhythmogenic adverse effects of cardiac glycosides. Cardiac glycosides (digitoxin) vs. Antioxidants and specific inhibitors was evaluated on Incidence of arrhythmogenic spontaneous Ca(2+) waves, ROS, and RyR2 thiol oxidation. In isolated rat ventricular myocytes, the cardiac glycoside digitoxin increased arrhythmogenic spontaneous Ca(2+) waves and RyR2 oxidation, effects prevented by antioxidants and specific inhibitors.
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