Effect of efonidipine hydrochloride (NZ-105), a dihydropyridine derivative with calcium antagonistic action, on myocardial oxygen tension in anesthetized dogs

• Published in: Nihon yakurigaku zasshi Vol. 108; no. 5; p. 267
• Main Authors: Fujikura, N, Yokoyama, T, Masuda, Y, Shikada, K, Tanaka, S
• Format: Journal Article
• Language: Japanese
• Published: Japan 1996
• Subjects: Animals; Blood Pressure - drug effects; Calcium Channel Blockers - pharmacology; Coronary Circulation - drug effects; Dihydropyridines - pharmacology; Dogs; Myocardium - metabolism; Nifedipine - pharmacology; Nisoldipine - pharmacology; Nitrophenols; Organophosphorus Compounds - pharmacology; Oxygen Consumption - drug effects; Partial Pressure
• ISSN: 0015-5691
• DOI: 10.1254/fpj.108.267

Effect of efonidipine hydrochloride (efonidipine) on myocardial oxygen tension (PO2) was investigated in open-chest anesthetized dog and compared with those of nifedipine and nisoldipine. PO2 was measured by a membrane-coated platinum wire, which was inserted into the myocardium. Intravenous administration of efonidipine (10 and 30 micrograms/kg) decreased mean blood pressure to a similar extent to that induced by nifedipine (1 and 3 micrograms/kg) or nisoldipine (1 and 3 micrograms/kg). Efonidipine increased coronary blood flow (CBF) and decreased the double product (DP) dose-dependently. Similar results were observed in nisoldipine-treated animals. Nifedipine produced a transient increase in CBF and a transient decrease in DP. The duration of action of efonidipine on CBF was longer than that of nifedipine or nisoldipine. Efonidipine increased PO2, and the effect was more pronounced in the endocardial region than in the epicardial region. Nifedipine had no significant effect on the PO2, while nisoldipine significantly increased PO2 in the endocardial region. The effect of efonidipine on the PO2 was greater than that of nisoldipine and the duration of action of efonidipine was longer than that of nisoldipine. These results suggest that efonidipine may increase PO2 by mediating, at least in part, a long-lasting increase in oxygen supply and a decrease in oxygen demand in dog heart.