Sakuji Shigematsu

Chapter 22 Role of ATP-Sensitive Potassium Channels in Ischemia/Reperfusion-Induced Ventricular Arrhythmias

Publisher Summary This chapter discusses the persistent activation of cardiac adenosine triphosphate (ATP)-sensitive potassium (K ATP ) channels during reperfusion on reperfusion induced-arrhythmias and on myocardial stunning, with the use of various antiarrhythmic and antidiabetic drugs that may or may not affect cardiac K ATP channels. In cardiac muscle, activation of K ATP channels shortens the duration of the action potential (APD), and in pancreatic β cells it inhibits the secretion of insulin. Thus, it is conceivable that drugs that modulate pancreatic K ATP channel should affect the incidence and severity of arrhythmias during the ischemia-reperfusion and those antiarrhythmic drugs capable of modulating cardiac K ATP channels would affect insulin secretion from pancreatic β cells. The electrophysiological effects of K ATP channel modulation during ischemia, and its implication for arrhythmogenesis, have been reviewed. However, little is known about how the modulation of K ATP channel activity during the reperfusion period affects the occurrence of postischemic ventricular arrhythmias.