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Cardioprotective effects of nicorandil on isoproterenol‐induced injury
Author(s) -
Ohta Hideyuki,
Azuma Junichi,
Tanaka Yuya,
Takihara Keiko,
Hamaguchi Tomoyuki,
Awata Nobuhisa,
Sawamura Akihiko,
Sperelakis Nicholas,
Kishimoto Susumu
Publication year - 1991
Publication title -
drug development research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.582
H-Index - 60
eISSN - 1098-2299
pISSN - 0272-4391
DOI - 10.1002/ddr.430220305
Subject(s) - nicorandil , isoprenaline , medicine , lactate dehydrogenase , vasodilation , endocrinology , creatine kinase , cyclic guanosine monophosphate , chemistry , guanosine , pharmacology , nitric oxide , enzyme , biochemistry , stimulation
Abstract Nicorandil, a new anti‐anginal drug, exerts a coronary vasodilation effect by mechanisms different from either nitrates or slow channel Ca + + entry blockers. This agent has been demonstrated to increase membrane K + conductance, elevate cyclic guanosine monophosphate content, and inhibit Ca + + kinetics in vascular smooth muscle cells. In the myocardium, however, the direct effects of the agent have not been elucidated. We examined whether nicorandil could antagonize myocardial injury in chick hearts induced by a toxic dose of isoproterenol. Isoproterenol treatment (240 mg/kg subcutaneously twice a day for 4 days) caused a significant increase in heart/body weight ratio and induced a remarkable histological perturbation. A substantial accumulation of Ca + + and a profound decrease of creatine kinase and lactate dehydrogenase activity were observed in the myocardium from isoproterenol‐treated chick. Oral administration of nicorandil (4 mg/day for 4 days, 15 min prior to each isoproterenol treatment) attenuated the deterioration induced by isoproterenol. The present study suggests that nicorandil partially protects the myocardium from the isoproterenol‐induced injury.