AQ-A 39 (5,6-dimethoxy-2-[3[[alpha-(3,4-dimethoxy)-phenylethyl]methylamino]propyl]phtalimidine), a specific bradycardic agent with direct action on the heart.

In isolated guinea-pig atria AQ-A 39 (5,6-dimethoxy-2[3[[alpha-(3,4-dimethoxy)-phenylethyl]methylamino]propyl]phtalimidine) decreased the rate of spontaneously beating preparations, the contraction amplitude and maximal driving frequency of electrically driven preparations. However, the concentrations which reduced the parameters by 30% were different: 1.4 microgram/ml, 110 microgram/ml and 19 microgram/ml respectively. The bradycardic action was not affected by atropine (0.05 microgram/ml). In the ECG of anaesthetized cats (0.1-10 mg/kg i.v.) the prominent effect of AQ-A 39 was the increase in heart period (PP') and QT in contrast to the chemically related verapamil which mainly increased PQ. Blood pressure and ejection time were slightly affected whereas the diastolic period was markedly prolonged (5 mg/kg i.v.). The 'triple product' of heart rate X ejection time X blood pressure was decreased by AQ-A 39. In cats with acute occlusion of a coronary artery branch, AQ-A 39 diminished the elevation of the ST-segment of the epicardial electrogram. AQ-A 39 decreased the heart rate in conscious dogs (5 mg/kg i.v.), provided the initial heart rate was higher than approximately 130 beats/min, but increased the heart rate when the initial rates were lower. The drug revealed an anticholinergic effect by antagonising the bradycardic action of carbachol on isolated atria from guinea pigs. The prevalent effect on heart rate differentiated AQ-A 39 from other drugs with direct action on the heart such as antiarrhythmics, the so-called 'calcium antagonists' and cholinergic drugs. The profile resembled that of alinidine (St 567) and indicated a decrease in myocardial oxygen demand.