Study of mechanism and effect of sodium 5-hydroxydecanoate on experimental ischemic ventricular arrhythmia

• Published in: Nihon yakurigaku zasshi Vol. 89; no. 3; p. 155
• Main Authors: Niho, T, Notsu, T, Ishikawa, H, Funato, H, Yamazaki, M, Takahashi, H, Tanaka, I, Kayamoto, M, Dabasaki, T, Yamasaki, F
• Format: Journal Article
• Language: Japanese
• Published: Japan 01-03-1987
• Subjects: Animals; Anti-Arrhythmia Agents - therapeutic use; Arrhythmias, Cardiac - prevention & control; Coronary Disease - drug therapy; Coronary Disease - metabolism; Decanoic Acids - pharmacology; Decanoic Acids - therapeutic use; Dogs; Energy Metabolism; Female; Guinea Pigs; Hydroxy Acids - pharmacology; Hydroxy Acids - therapeutic use; Ion Channels - drug effects; Male; Myocardium - metabolism; Potassium - metabolism; Rats; Rats, Inbred Strains; Tachycardia - prevention & control; Ventricular Fibrillation - prevention & control
• ISSN: 0015-5691

We investigated the effects of sodium 5-hydroxydecanoate (5-HD) on experimentally induced ischemic arrhythmia and its mechanisms of action by biochemical and electrophysiological techniques. 5-HD, at the single dose of 200 mg/kg (p.o.) or at the one week multiple doses of 3 to 100 mg/kg (p.o.), suppressed the incidence of ventricular fibrillation induced by coronary ligation in rats. 5-HD at the dose of 3 or 10 mg/kg (i.v.) elevated the ischemically decreased ventricular fibrillation threshold in the coronary ligated dogs. In isolated rat heart, 5-HD suppressed the K+ release from ischemic myocardium at the doses of 10(-5) to 10(-3) M. 5-HD at the dose of 10(-4) M decreased the open state probability of ATP regulated K+ channel in isolated myocardial cell of guinea pig. Contents of high-energy-phosphate compounds were markedly decreased in ischemic myocardium of rats, and they were not affected by 5-HD. These results demonstrate the efficacy of 5-HD against experimental ischemic ventricular arrhythmia. Its antiarrhythmic action may be attributed, at least in part, to the suppression of K+ release from ischemic myocardium by possibly inhibiting the ATP regulated K+ channel.