Fiedler V B, Nitz R E
Basic Res Cardiol. 1982 May-Jun;77(3):270-7. doi: 10.1007/BF01908042.
The intravenous effects of molsidomine on the coronary circulation, myocardial oxygen consumption, and hemodynamics were investigated in anesthetized, open-chest dogs. Left coronary artery flow was reduced after drug administration, while coronary resistance remained unaffected. The coronary arteriovenous oxygen difference did not change after molsidomine. Myocardial oxygen consumption was significantly reduced. Stroke work of the heart was diminished. Molsidomine caused a dose-dependent decrease in aortic and left ventricular pressures (after-load) as well as a sustained fall in left ventricular end-diastolic and mean pulmonary artery pressures (preload). Heart rate and contractility were only moderately affected. Stroke volume and cardiac output decreased significantly for the experimentation time, while total peripheral resistance increased after 0.25 mg/kg molsidomine. All observed effects of the drug can be explained by extracardiac effects: an increase in venous capacity. No direct effects of molsidomine on myocardial function could be noted. The fall in blood pressure was not induced by vasodilatation of peripheral arteriolar vessels but occurred as sequel of the reduced cardiac output following decreased ventricular filling. Molsidomine improved the oxygen supply-demand balance by decreasing external work of the heart and hence myocardial oxygen demand.
