[A study of the mechanism of the action of Bunaphtine recording the myocardial monophasic action potentials in man. Conclusive report (author's transl)]

Abstract

In this paper the authors conclude their study of the mechanism of the action of Bunaphtine. Both atrial and ventricular MAP were recorded by a suction electrode in 13 patients before and after Bunaphtine (1.5-2 and 2.5 mg/Kg i.v.). With the lower dosages, the drug acts specifically on repolarization: it greatly increases the duration of MAP, together with a proportional ERP prolongation; the ERP/MAP ratio is not changed. With the higher dosages, there is a greater effect on the depolarization velocity (decrease of the O dv/dt phase of MAP) and on the conduction, this last being less evident. At the atrial level there is a conspicous ERP prolongation, with a remarkable increase of ERP/MAP ratio. There is full agreement between these results and those obtained experimentally on the dog and in vitro. Bunaphtine has therefore unquestionable antiarrhythmic properties and it can have a double action mechanism; with higher dosages its action-quinidine-like-is predominant at the atrial level.