Protection of Chlorpromazine-Induced Arrhythmia by Flavin-Adenine-Dinucleotide in Canine Heart

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Abstract
To investigate the mechanism of chlorpromazine (CPZ)-induced ventricular arrhythmia the changes in ventricular fibrillation threshold (VFT) were followed after i.v. injection of CPZ (1 mg/kg) in dogs. Following injection VFT was decreased to 56.6 .+-. 5.4% (mean .+-. SE) of the initial level. Since FAD combines specifically with CPZ in vitro whether prior treatment with FAD prevents the CPZ effect was investigated. With FAD (2 mg/kg) and CPZ-induced decrease in VFT was significantly cancelled (92.2 .+-. 4.2% of the initial level). Mitochondria isolated from canine heart after CPZ injection showed a significant decrease in respiratory control index and ADP/O. Effects of CPZ on canine heart mitochondria were well cancelled by prior administration of FAD. The arrhythmogenic action of CPZ might be associated in part with impaired function of heart mitochondria. FAD may be useful in the treatment of the cardiac disturbances associated with overdosage of CPZ.