ROLE OF POTASSIUM CHANNELS IN HALOTHANE-EPINEPHRINE ARRHYTHMIAS

It has been reported that antiarrhythmic drugs possessing the property of potassium channel blockade were most effective in preventing halot hane-epiephrine induced arrhythmias. Recent attention has focused on A TP-sensitive potassium (K-ATP) channels because of their contribution to the cardiovascular actions of volatile anesthetics. The present stu dy was designed to evaluate whether K-ATP channels or transient outwar d potassium channels (Ito) were involved in the mechanism of halothane -epinephrine arrhythmias in rat. Rats were anesthetized with halothane (1.5%), and the lungs were mechanically ventilated. The arrhythmogeni c thresholds of epinephrine during halothane anesthesia were determine d in 74 rats receiving saline or one of tested agents. The anhythmogen ic dose of epinephrine (ADE) was significantly increased by a K-ATP ch annel opener, JTV506 (P < 0.01), and had a tendency to be increased by other K-ATP channel openers, cromakalim, nicorandil, KRN2391 and Y 26 763, but were not affected by a K-ATP channel blocker, glibenclamide. The Ito blocker, 4-aminopyridine, also significantly increased the ADE . Epinephrine produced second-degree or complete atrioventricular bloc k in 4 out of 74 rats receiving glibenclamide. These results suggest t hat Ito but not K-ATP channels might be involved in the mechanism in p roducing halothane-epinephrine arrhythmias.