Nicorandil suppresses early afterdepolarisation and ventricular arrhythmias induced by caesium chloride in rabbits in vivo

Abstract

Nicorandil suppresses the early afterdepolarisations and ventricular tachyarrhythmias induced by Cs, possibly by increasing the membrane K conductance.

Nicorandil Suppresses a Hump on the Monophasic Action Potential and Torsade de Pointes in a Patient with Idiopathic Long QT Syndrome.

“…Our findings are in agreement with some experimental reports, [8][9][10] and the hump on MAP and ventricular arrhythmia in this case were suppressed after the administration of the K-channel opener nicorandil. A shortening of the QT interval was concomitantly observed, and transient discontinuation of the drug resulted in a prolongation of the QT interval.…”

Effect of Constant and Intermittent Vagal Stimulation on the Heart Rate and Heart Rate Variability in Rabbits.

“…Adult Japanese white male rabbits (weight, 2.5 to 3.3 kg) were anesthetized with intraperitoneal secobarbital sodium (20 mg/kg) and injected with additional intravenous doses as needed to maintain a constant level of anesthesia throughout the course of the experiment. Animals were instrumented as described previously [16]. In brief, mechanical ventilation with room air was performed with a ventilator (SN-480-5, Shinano, Tokyo, Japan) through a tracheal cannula at a constant rate of 52 breaths/min (0.86 Hz).…”

“…The standard limb-lead ECG (lead II) and femoral arterial BP were monitored. Monophasic action potentials (MAPs) from the left ventricular endocardium were recorded by the contact electrode technique as described previously [16].…”

Baroreflex Sensitivity Predicts the Induction of Ventricular Arrhythmias by Cesium Chloride in Rabbits

“…1 In animal experiments, intravenous cesium chloride (Cs) administration produces EADs in the ventricular monophasic action potentials (MAPs) and causes both prolongation of the QT interval and polymorphic ventricular tachycardias (PVTs) resembling torsade de pointes. [2][3][4][5][6][7] The electrocardiographic changes and ventricular arrhythmias induced by Cs are considered to represent an experimental animal model of the long QT syndrome. [2][3][4] Torsade de pointes associated with the long QT syndrome is often elicited by sudden increases in sympathetic activity 8 and can be suppressed by -adrenergic blocking agents 9 or by ablation of the left stellate ganglion.…”