van Ackern K, Deuster J E, Mast G J, Schmier J
Arzneimittelforschung. 1975 Jun;25(6):891-6.
The effect of amantadine-hydrochloride on heart and circulation is studied in 7 anesthetized, otherwise normal dogs with a mean body weight of 27.2 kg and in 8 heart-lung preparations of dogs. Arterial blood pressure, right atrial pressure, cardiac output and heart rate are measured and continuously monitored. Stroke volume and peripheral resistance are calculated. Left ventricular peak- and enddiastolic pressure, the rate of rise of intraventricular pressure and t-dp/dt are additionally measured in the heart-lung-preparations. Below 3 mg with kg(-1) in anesthetized dogs and 10 mg in the heart-lung preparation, respectively, a positive inotropic effect of amantadine is observed. This effect is caused by a liberation of catecholamines. Higher dosage of amantadine decreases cardiac contractility significantly. Therefore the negative inotropic influence of the drug itself has to be distinguished from the indirect sympathomimetic effect resulting from local release of myocardial catecholamines. Cardiac arrhythmias which occur in several experiments, can mostly be eliminated with propranolol or other drugs like lidocaine or sparteinsulphate.