Key result
Nicorandil nearly doubles ischemic APD90 shortening without increasing ventricular fibrillation risk.
Why the study?
Nicorandil is a nitrovasodilator that opens myocardial KATP channels in vitro, but its effects on ischemia-induced MAP shortening, potassium accumulation, and arrhythmia occurrence at clinical doses were unclear.
Does nicorandil augment regional ischemia-induced monophasic action potential shortening and potassium accumulation without causing serious proarrhythmia in anesthetized open-chest dogs?
Population
Anesthetized open-chest dogs undergoing repeated 5-minute LAD occlusion
Comparison
Nicorandil (0.2-0.5 mg/kg i.v. before third occlusion) vs second occlusion control
Design
Preclinical experimental study with repeated ischemia-reperfusion in same animals
Authors
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Supports KATP activation without proarrhythmia in canine ischemia; hypothesis-generating for human cardioprotection.
Does nicorandil augment regional ischemia-induced monophasic action potential shortening and potassium accumulation without causing serious proarrhythmia in anesthetized open-chest dogs?
Absolute Event Rate: 25% vs 13%
Nicorandil at clinical doses facilitates regional ischemia-induced activation of myocardial KATP channels without causing serious proarrhythmia, potentially protecting the myocardium against ischemia/reperfusion damage.
Miyazaki et al. (1995) studied Regional myocardial ischemia (n=25). Nicorandil vs. Second occlusion (control without nicorandil) was evaluated on Occlusion-induced shortening of monophasic action potential duration at 90% repolarization (APD90). Nicorandil augmented ischemia-induced APD90 shortening (25% vs 13%) and extracellular potassium increase without increasing the prevalence of ventricular fibrillation (4% vs 20%).
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