Effects of catecholamines on cardiovascular actions of molsidomine in anesthetized dogs.

We measured over a 2-h period the effects of molsidomine (0.5 mg/kg i.v.) on pulmonary artery and left ventricular (LV) end-diastolic pressures and internal heart dimension (preload), LV systolic and peripheral blood pressures and total peripheral resistance (afterload), and heart rate, LV dP/dt, stroke volume, and cardiac output (heart performance) of dogs anesthetized with pentobarbital. The hemodynamic effects of molsidomine were influenced by intravenous infusion of 0.10 or 0.20 micrograms/kg/min norepinephrine or 3 or 6 micrograms/kg/min dopamine. Molsidomine decreased preload, stroke volume, and cardiac output for over 2 h and ventricular and peripheral pressures for 45 min. Peripheral resistance, heart rate, and LV dP/dtmax were not altered. Low doses of norepinephrine and dopamine reversed the effect of molsidomine on afterload. However, neither catecholamine influenced the reduced end-diastolic filling pressure after molsidomine. The diminished stroke volume was elevated by either catecholamine so that cardiac output eventually increased. These results indicate that both norepinephrine and dopamine can reverse the certain effects of intravenously administered molsidomine, probably by increasing cardiac contractile force, cardiac output, and peripheral resistance. A combination of molsidomine's preload lowering effects with dopamine's effects on afterload may be useful for the treatment of patients with myocardial failure.