Cellular and ionic mechanisms underlying the effects of cilostazol, milrinone, and isoproterenol to suppress arrhythmogenesis in an experimental model of early repolarization syndrome
Keywords: جریان پتاسیم بیرون گذرا; Phosphodiesterase-3 inhibitors; Transient outward potassium current; Pharmacology; Ventricular fibrillation; Sudden cardiac death; Electrophysiology; Early repolarization