771-1 Role of Intracellular Calcium In the Antiarrhythmic Effect of Procalnamide During Ventricular Fibrillation In Rat Hearts

Intracellular calcium ([Ca 2+ ]i) overload is considered one of the factors that cause ventricular fibrillation (VF). In addition, VF itself causes and maintains [Ca 2+ ]i overload. We tested whether the class IA antiarrhythmic agent procainamide can reduce [Ca 2+ ]i overload during VF and if so, whether such reduction is responsible for the recovery of left ventricular function. For this purpose, we measured the effects of 0.1 mM (0.03 mg/ml) procainamide perfusion on left ventricular developed pressure (LVP), heart rate, and [Ca 2+ ]i during pacing-induced VF in isolated rat hearts. [Ca 2+ ]i was assessed by surface fluorometry after Indo-1/AM-loading. The concentration of procainamide was selected in a way that about half of the hearts would recover from VF (criteria: recovery of LVP g 67%). During perfusion with 0.1 mM procainamide, 6 hearts recovered from VF (●), whereas 8 hearts did not recover (z, recovery of LVP l 33%). In the untreated control group (○, n = 5), no heart recovered from VE Procainamide effects on heart rate (left panel) and [Ca 2+ ]i (right panel) are shown (mean ± SEM; † p l .05 vs. control; * p l 0.05 vs. no recovery): Download high-res image (109KB) Download full-size image We conclude that procainamide can reduce [Ca 2+ ]i overload during VF. In addition, the reduction of the [Ca 2+ +] i overload might be responsible for the recovery of the left ventricular function. This reduction appeared to be dependent on the fibrillation rate (use-dependent) rather than on the decrease of heart rate.