| Abstract: | ![]()
Abstract The mode of action of a calcium-antagonistic drug, nifedipine, on the spontaneously beating, isolated, perfused rat heart was studied at two different calcium concentrations of the Ringer solution, [Ca++]o, (2.0 and 5.0 meq./l). The sinus node discharge, the aortic pressure amplitude and hence the work index were greater at 5.0 than at 2.0 meq./l. Nifedipine 100 μg/1 caused a reduction in these parameters, the effects being most pronounced at the lowest [Ca++]o studied. ECG tracings demonstrated that the PR-interval was longer at 2.0 than at 5.0 meq./l of calcium. The AV conduction time further increased after the addition of nifedipine. This effect was enhanced at the lowest [Ca++]o used, where varying degrees of AV block occurred in several experiments. The drug also reduced the R-wave voltage and the RT-interval. Calcium-induced ventricular tachyarrhythmias were produced, which were suppressed by nifedipine. Nifedipine 100 μg/l produced a small and transient increase in the coronary flow, but a tremendous increase in the ratio coronary flow/work index was observed. This indicates improvement of the cardiac energy balance caused by an increase in the coronary oxygen supply in relation to the myocardial oxygen demand. |
