Electrophysiological and cardiohemodynamic effects of a new type of calcium channel blocker AH-1058 assessed by the canine in vivo model

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  • Takahara Akira
    Pharmaceutical Research Laboratories,Ajinomoto Co.,Inc.,1-1 Suzuki-cho,Kawasaki-ku,Kawasaki 210-8681,Japan
  • Sugiyama Atsushi
    Department of Pharmacology,Yamanashi Medical University,Tamaho-cho,Nakakoma-gun,Yamanashi 409-3898,Japan
  • Dohmoto Hideki
    Pharmaceutical Research Laboratories,Ajinomoto Co.,Inc.,1-1 Suzuki-cho,Kawasaki-ku,Kawasaki 210-8681,Japan
  • Yoshimoto Ryota
    Pharmaceutical Research Laboratories,Ajinomoto Co.,Inc.,1-1 Suzuki-cho,Kawasaki-ku,Kawasaki 210-8681,Japan
  • Hashimoto Keitaro
    Department of Pharmacology,Yamanashi Medical University,Tamaho-cho,Nakakoma-gun,Yamanashi 409-3898,Japan

書誌事項

タイトル別名
  • Electrophysiological and Cardiohemodynamic Effects of AH-1058, a New Type Calcium Channel Blocker, Assessed by the In Vivo Canine Model.

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抄録

AH−1058(4−(5H−dibenzo[a, d]cyclohepten−5−ylidene)−1−[(E)−3−(3−methoxy−2−nitro)phenyl−2−propenyl]piperidine hydrochloride)is a novel calcium channel blocker whose chemical structure is quite different from those of typical calcium channel blockers.In this study, electrophysiological and hemodynamic effects of AH−1058 were assessed in the halothane−anesthetized, closed−chest canine model.Intravenous administration of a canine antiarrhythmic dose of 100 μg/kg of AH−1058(n=6)did not affect the cardiovascular variables, except that the cardial output was decreased at 30 min after the drug administration.Additional administration of 200 μg/kg of AH−1058(n=6)suppressed the sinus nodal automaticity, AV nodal conduction and ventricular contraction and decreased the mean blood pressure, cardiac output and double product.The effects gradually appeared, while no change was detected in the intraventricular conduction, ventricular repolarization period, ventricular effective refractory period, preload to the left ventricle and total peripheral vascular resistance during the observation period of 30 min.The cardiosuppressive effects of AH−1058 can be explained by its calcium channel blocking action demonstrated in a previous in vitro experiment, while the lack of the effect on the vascular resistance would suggest that AH−1058 may become a slow−acting cardioselective calcium channel blocker.

収録刊行物

  • Jpn.J.Pharmacol.

    Jpn.J.Pharmacol. 83 (2), 107-112, 2000

    公益社団法人 日本薬理学会

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