NATURE OF [CA2-FIBRILLATION AND QUINIDINE TREATMENT IN PERFUSED RAT HEARTS(](I) TRANSIENTS DURING VENTRICULAR)

Citation
S. Kojima et al., NATURE OF [CA2-FIBRILLATION AND QUINIDINE TREATMENT IN PERFUSED RAT HEARTS(](I) TRANSIENTS DURING VENTRICULAR), The American journal of physiology, 266(4), 1994, pp. 80001473-80001484
Citations number
43
Categorie Soggetti
Physiology
ISSN journal
00029513
Volume
266
Issue
4
Year of publication
1994
Part
2
Pages
80001473 - 80001484
Database
ISI
SICI code
0002-9513(1994)266:4<80001473:NO[AQT>2.0.ZU;2-3
Abstract
We studied intracellular Ca2+ concentration ([Ca2+](i)) and the electr ocardiographic 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 (F-400/F-510) and exp ressed as a percentage of the control amplitude of F-400/F-510 transie nts. F-400/F-510 increased to similar to 250% during 2- (n = 14) or 20 -min (n = 9) VF. Quinidine significantly decreased F-400/F-510 by 60% after 2-min VF; however, this effect was blunted after 20-min VF. Afte r 2-min VF, F-400/F-510 and left ventricular pressure recovered almost to the control level. However, recovery of F-400/F-510 and ventricula r function was poor after 20-min VF. The relationship between [Ca2+](i ) and the electrocardiogram (ECG) during VF was evaluated by power spe ctrum analysis of F-400/F-510 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 ve ntricular 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 th e [Ca2+](i) transients was 19 Hz. During quinidine treatment, the VF r ate decreased significantly, and clear [Ca2+](i) transients were noted in all records responding to every one or two ECG signals. The conclu sions were the following: 1) [Ca2+](i) responds to electrical signals rapidly (up to 19 Hz) during VF. This fast [Ca2+](i) response is a pro bable 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) tr ansients rates. 3) 20-min VF caused [Ca2+](i) overload and poor functi onal recovery after defibrillation.