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

Intracellular calcium ([Ca2+]i) overload is considered one of the factors that cause ventricular fibrillation (VF). In addition, VF itself causes and maintains [Ca2+]i overload. We tested whether the class IA antiarrhythmic agent procainamide can reduce [Ca2+]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 0.1mM (0.03mg/ml) procainamide perfusion on left ventricular developed pressure (LVP), heart rate, and [Ca2+]i during pacing-induced VF in isolated rat hearts. [Ca2+]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>67%). During perfusion with 0.1mM procainamide, 6 hearts recovered from VF (●), whereas 8 hearts did not recover (&z.squf;, recovery of LVP<33%). In the untreated control group (○, n=5), no heart recovered from VE Procainamide effects on heart rate (left panel) and [Ca2+]i (right panel) are shown (mean±SEM; †p<.05 vs. control; *p<0.05 vs. no recovery):We conclude that procainamide can reduce [Ca2+]i overload during VF. In addition, the reduction of the [Ca2++]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