Haemodynamic effects of molsidomine.

The haemodynamic effects of N-carboxy-3-morpholino-sydronimine-ethylester (molsidomine, SIN 10, Corvaton) were studied in anaesthetized mongrel dogs. The effects of molsidomine were identical when given i.v. or i.d. Because of the lack of difference in activity with similar doses i.v. or i.d. complete absorption of the drug can be assumed. There was a sustained decrease in arterial blood pressure accompanied by a long lasting decrease in left ventricular enddiastolic and mean pulmonary artery blood pressure. Heart rate was only moderately affected. Left ventricular endsystolic and enddiastolic volumes, as estimated from measurements of left ventricular outer dimension with ultrasonic techniques, decreased. Even in nearly toxic doses molsidomine did not influence left ventricular contractility as judge from measurements of dp/dt max., (dp/dt)/(LVP-LVEDP + c) max., ejection time and duration of systole. All the observed effects of molsidomine can be explained by an extracardiac action: increase in systemic venous capacity. Consequently venous return, mean pulmonary artery pressure and left ventricular filling pressure are reduced leading to a decrease in left ventricular volumes. This should cause a reduction of cardiac output, of peripheral blood pressure and of external cardiac work. In connection with reduced left ventricular wall tension a fall in myocardial oxygen consumption can be expected.