Nature of Ca2+i transients during ventricular fibrillation and quinidine treatment in perfused rat hearts

We studied intracellular Ca2+ concentration (Ca2+i) and the electrocardiographic signals during pacing-induced ventricular fibrillation (VF) and quinidine treatment (0.4 mg/min) using surface fluorometry in indo 1-acetoxymethyl ester (AM)-loaded perfused rat hearts. Ca2+i was evaluated as the indo 1 fluorescence ratio (F400/F510) and expressed as a percentage of the control amplitude of F400/F510 transients. F400/F510 increased to approximately 250% during 2- (n = 14) or 20-min (n = 9) VF. Quinidine significantly decreased F400/F510 by 60% after 2-min VF; however, this effect was blunted after 20-min VF. After 2-min VF, F400/F510 and left ventricular pressure recovered almost to the control level. However, recovery of F400/F510 and ventricular function was poor after 20-min VF. The relationship between Ca2+i and the electrocardiogram (ECG) during VF was evaluated by power spectrum analysis of F400/F510 and ECG signals. During VF (25 +/- 3 Hz) with high irregularity, there were no clear Ca2+i transients (n = 110). When the cardiac rhythm (22 +/- 3 Hz) was regular, including ventricular tachycardia, there were recognizable Ca2+i signals with dominant frequencies that were the same (n = 2), one-half (n = 12), or one-third (n = 1) of the ECG frequencies. The highest frequency of the Ca2+i transients was 19 Hz. During quinidine treatment, the VF rate decreased significantly, and clear Ca2+i transients were noted in all records responding to every one or two ECG signals. The conclusions were the following: 1) Ca2+i responds to electrical signals rapidly (up to 19 Hz) during VF. This fast Ca2+i response is a probable cause of high Ca2+i during VF. 2) Quinidine decreased Ca2+i after 2-min VF possibly in part by slowing the VF and Ca2+i transients rates. 3) 20-min VF caused Ca2+i overload and poor functional recovery after defibrillation.