The effects of nicorandil on electrophysiological changes in acute myocardial ischemia and reperfusion.
This study was undertaken to clarify the effects of nicorandil on electrophysiological changes during acute ischemia and following reperfusion. We prepared an acute ischemic heart model by ligating the left anterior descending coronary artery in 27 dogs. After 10 minutes, reperfusion was performed. The changes in ventricular effective refractory period (ERP) and intramyocardial conduction time (ICT) were compared between the nicorandil group (n = 12) which received nicorandil intravenously before the coronary ligation and the control group (n = 15). In the control group, the ERP was shortened during ischemia, and rapidly shortened immediately after reperfusion, but was slightly prolonged 10 minutes after reperfusion. The ICT was prolonged during ischemia, but returned to the pre-ischemia value after reperfusion. In the nicorandil group, the changes in ERP and ICT were significantly inhibited compared to those in the control group. The incidence of ventricular fibrillation (VF) during reperfusion was 42% in the control group. However, there was no VF during reperfusion in the nicorandil group. Therefore, nicorandil may correct both the delayed conduction and the uneven ventricular effective refractory period detected during acute ischemia and following reperfusion, inhibiting the development of ventricular arrhythmia during reperfusion.
Shinohara
H
H
Second Department of Internal Medicine, School of Medicine, University of Tokushima, Japan.
Nishikado
A
A
Wakatsuki
T
T
Sakabe
K
K
Ito
S
S
D000208:Acute Disease; D000818:Animals; D000889:Anti-Arrhythmia Agents / Q000627:therapeutic use*; D004195:Disease Models, Animal; D004285:Dogs; D004353:Drug Evaluation, Preclinical; D004594:Electrophysiology; D017202:Myocardial Ischemia / Q000150:complications / Q000188:drug therapy* / Q000503:physiopathology; D015428:Myocardial Reperfusion Injury / Q000150:complications / Q000188:drug therapy* / Q000503:physiopathology; D009536:Niacinamide / Q000031:analogs & derivatives* / Q000627:therapeutic use; D020108:Nicorandil; D015221:Potassium Channels / Q000819:agonists*; D014693:Ventricular Fibrillation / Q000188:drug therapy / Q000209:etiology / Q000503:physiopathology
D000889:Anti-Arrhythmia Agents; D015221:Potassium Channels; D009536:Niacinamide; D020108:Nicorandil