Cardiohemodynamic effects of nitroglycerin and several vasodilators.

The cardiohemodynamic effects of antianginal drugs and typical vasodilators, namely nitroglycerin, N-nitroso-morpholino-aminoacetonitrile (SIN-1A), aminophylline, papaverine, trapymin, dipyridamole, carbochromene, nifedipine, etafenone, prenylamine and iproveratril, were comparatively studied in anesthetized open-chest dogs. These drugs all decreased the systemic blood pressure, although aminophylline, papaverine and trapymin induced a marked increase after an initial transient fall. Changes in the total cardiac output represented by the blood flow in the pulmonary artery were quite similar to those in the venous return (VR), sum of the inferior and superior caval flow. The contribution of the superior caval flow to the change in VR was less than that of the inferior caval flow. Changes in the right atrial pressure (RAP) were far less than those in VR, but both the RAP and VR were dose-dependently modified by these drugs. I) Nitroglycerin and SIN-1A caused decreases in both the VR and the RAP and transient increases in the heart rate (HR). IIa) Aminophylline, papaverine and trapymin increased the VR, decreased the RAP and produced a long-lasting tachycardia. IIb) Dipyridamole increased the VR and induced a barely recognizable change in the RAP and the HR. Carbochromene induced similar changes but bradycardia was more evident. IIc) Nifedipine, etafenone and prenylamine increased the VR but simultaneously raised the RAP and induced bradycardia. A large dose over the therapeutic range turned the increase of VR into a marked decrease. IId) Iproveratril decreased the VR but markedly increased the RAP and caused bradycardia. It is concluded that antianginal drugs are clearly differentiated from the other vasodilators and that the latter agents can be classified into 4 groups, judging from the drug effects on the relations between the VR and RAP.