Effects of activation sequence on monophasic action potential configuration in the dog

• Published in: Journal of electrocardiology 1997, Vol.30 (1), p.65-70
• Main Authors: Tachibana, Hidetada, Kubota, Isao, Yamaki, Michiyasu, Kondo, Tsunehiro, Tomoike, Hitonobu
• Format: Article
• Language: English
• Subjects: 4-Aminopyridine - pharmacology; Action Potentials - drug effects; Action Potentials - physiology; Animals; Biological and medical sciences; Cardiac dysrhythmias; cardiac memory; Cardiology. Vascular system; Dogs; Electric Stimulation; Electrocardiography - drug effects; electrotonic interaction; Heart; Heart Ventricles - drug effects; Medical sciences; monophasic action potential; transient outward current 4-aminopyridine; Ventricular Function
• ISSN: 0022-0736; 1532-8430
• DOI: 10.1016/S0022-0736(97)80036-2

The effects of altered activation sequence on the monophasic action potential (MAP) in in situ beating hearts are not known, although its effects on refractory periods are well documented. In nine anesthetized, openchest dogs, complete atrioventricular block was produced, and the heart was driven by either right ventricular or left ventricular stimulation. The MAPs of the right and left ventricles were recorded by contact electrodes at cycle lengths of 1,000, 800, 600, and 400 ms. The MAP configuration was evaluated with regard to the difference between phase 1 and phase 2 MAP amplitudes and MAP duration at 50 and 90% repolarization. An MAP recorded from the ventricle that was being electrically stimulated was designated an ipsilateral ventricular stimulation, whereas the MAP recorded from the nonstimulated ventricle was termed a contralateral ventricular stimulation. The difference in amplitude and the 50% and 90% MAP durations for ipsilateral ventricular stimulation were consistently larger than for contralateral ventricular stimulation at all cycle lengths tested. Transient outward current did not appear to play a major role in producing such differences in MAP because intravenous treatment with 4-aminopyridine, a blocker of transient outward current, did not affect the configuration of the MAP. These findings provide an insight on the influence of ventricular activation sequence on the shape of the transmembrane action potential.