Effects of nicardipine, a new dihydropyridine vasodilator, on coronary circulation and ischemia-induced conduction delay in dogs.

The effects of 2,6-dimethyl-4-(3-nitrophenyl)-1,4-dihydropyridine-3,5-dicarboxylic acid 3-[2-(N-benzyl-N-methylamino)]ethyl ester 5-methyl ester hydrochloride (nicardipine, YC-93), a new potent calcium antagonistic coronary vasodilator, on coronary circulation and ischemia-induced conduction delay were examined in anesthetized open-chest dogs. Nicardipine increased both the coronary flow and regional myocardial blood flow in the pre-ischemic period in a dose-dependent manner. However, nicardipine in a dose of 30 micrograms/kg, which was sufficient to enhance the coronary circulation almost maximally, failed to reduce the conduction delay produced by coronary occlusion under a constant atrial pacing. A high dose of nicardipine (300 micrograms/kg) enough to exert a slow channel blocking action on the cardiac tissue was required to improve the conduction delay. These results suggest that the coronary vasodilating action of the calcium antagonists is unlikely to play an essential role in reducing the conduction delay in the ischemic myocardium.