During hypokalemia, IKAS activation plays a protective role by maintaining repolarization reserve, whereas its blockade facilitates the induction of ventricular fibrillation.
Hypokalemia activates IKAS to shorten APD and maintain repolarization reserve at late activation sites during ventricular pacing. IKAS blockade prominently lengthens the APD at late activation sites and facilitates ventricular fibrillation induction.
Chan et al. (Sat,) studied this question.
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