Genetic defects in sodium channel-related genes can cause a loss- or gain-of-function of sodium channel current (INa) leading to the manifestation of various disease phenotypes, including Brugada syndrome, long QT syndrome, progressive cardiac conduction disease, sick sinus syndrome, multifocal ectopic Purkinje-related premature contractions, and atrial fibrillation [3]. Nicainoprol is a fast-sodium-channel blocking drug, which is a potent antiarrhythmic agent. In isolated working rat hearts, nicainoprol (1 μM, 5 μM and 10 μM) induced concentration-related protection against reperfusion arrhythmia without changing the cardiodynamics. Given to anesthetized rats, nicainoprol (5 and 10 mg/kg i.v.) reduced dose dependently in the early post occlusion (0-30 min) period, the percentage of animals with premature ventricular complexes (PVCs) and ventricular tachycardia while completely preventing the occurrence of ventricular fibrillation. 5 or 10 mg/kg nicainoprol induced a decrease in heart rate, blood pressure and myocardial oxygen consumption. The ratio of infarct mass to ventricular mass was significantly reduced by 20% at a dose of 5 mg/kg and by 28% at the dose of 10 mg/kg. Thus, nicainoprol could be useful in the prevention and treatment of arrhythmias associated with acute myocardial infarction[4]. The intranodal conduction time (p ≤ 0.01) and the infranodal conduction time (p ≤ 0.001) increased, and the QRS duration (p ≤ 0.05) lengthened significantly even during 1 mg/kg/h intravenous administration of nicainoprol[5]. 1.5-2 mg/kg nicainoprol successfully terminated the tachycardia in 17 patients due to block in the retrograde tachycardia limb in 15 and the antegrade limb in 2 patients. Prolongation of the cycle length preceded the termination in each case[6].
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