Why the study?
Does nicardipine affect cardiac contraction and heart rate in a cross-perfused canine atrium model?
Does nicardipine affect cardiac contraction and heart rate in a cross-perfused canine atrium model?
Nicardipine acts as a calcium antagonist with cardiac depressant properties, independent of phosphodiesterase inhibition in cardiac tissues.
Nicardipine shows direct cardiac effects in canine models; leaves open translation to human practice or differentiation from verapamil.
Effects of nicardipine, a newly synthesized dihydropyridine vasodilator exhibiting cyclic phosphodiesterase inhibitory properties, were studied in the isolated canine atrium which was cross-perfused with blood from a donor dog. When nicardipine (1.0-10 micrograms/kg) was administered intravenously to the donor dogs, the systemic blood pressure decreased and the heart rate did not significantly change. However, the contraction and beat rate of the isolated atrium were only slightly decreased. At larger doses (30-100 micrograms/kg, i.v.), the systemic blood pressure fell markedly and was usually accompanied by marked bradycardia, which was greater than that of the isolated atrium. Nicardipine injected into the sinus node artery of the isolated atrium caused dose-related negative chronotropic and inotropic effects which were less pronounced than those of verapamil. In contrast, papaverine increased right atrial rate and contractile force. Nicardipine similarly to verapamil and unlike manganese ion caused greater inhibition of the right atrial contraction at higher than lower pacing frequencies. From these results, it is concluded that nicardipine may produce predominantly cardiac depressant properties as a calcium antagonistic, and that such may not be related to phosphodiesterase inhibition in cardiac tissues.
No takes yet. Share an insight, caveat, or question.
Watanabe et al. (1981) studied this question.
Synapse has enriched 2 closely related papers on similar clinical questions. Consider them for comparative context: