title: Role of ATP-sensitive K+ channel on ECG ST segment elevation during a bout of myocardial ischemia. A study on epicardial mapping in dogs.
abstract: BACKGROUND
  ATP-sensitive K+ channels are activated when the myocardium becomes ischemic. However, the role of the ATP-sensitive K+ current in the emergence of ECG ST changes during ischemia remained unclarified.
  
  
  RESULTS
  The left anterior descending coronary artery (LAD) was cannulated and perfused with arterial blood from the carotid artery through a bypass tube in 8 anesthetized, open-chest dogs. An array of 60 unipolar electrodes mounted on a sock was used to record epicardial electrograms of the whole heart. Pinacidil (10 micrograms.kg-1 x min-1), an ATP-sensitive K+ channel opener, was infused into the bypass tube for 2 minutes, and the electrograms were recorded before and after the infusion. The elevation of the ST segment and the increase of QRST area were observed spatially over the LAD-perfused region. At the electrode showing the largest ST segment elevation, the activation recovery interval, an index of action potential duration, was shortened from 202 +/- 9 to 111 +/- 18 milliseconds (P < .001). These electrographic changes were similar to those noted in 2-minute coronary occlusion (n = 8). The extent of ST segment elevation during coronary occlusion was attenuated after the intravenous pretreatment with glibenclamide (0.3 mg/kg), a blocker of the KATP channel (n = 5).
  
  
  CONCLUSIONS
  The findings of this study suggest that the activation of ATP-sensitive K+ channels during a bout of acute myocardial ischemia plays an important role in the emergence of ECG ST elevation.
authors.affiliation: First Department of Internal Medicine, Yamagata University School of Medicine, Japan.
authors.forename: I
authors.initials: I
authors.lastname: Kubota
authors.forename: M
authors.initials: M
authors.lastname: Yamaki
authors.forename: T
authors.initials: T
authors.lastname: Shibata
authors.forename: E
authors.initials: E
authors.lastname: Ikeno
authors.forename: Y
authors.initials: Y
authors.lastname: Hosoya
authors.forename: H
authors.initials: H
authors.lastname: Tomoike
mesh_terms: D000200:Action Potentials / Q000502:physiology; D000255:Adenosine Triphosphate / Q000502:physiology*; D000818:Animals; D004285:Dogs; D004562:Electrocardiography / Q000379:methods*; D005905:Glyburide / Q000494:pharmacology; D006146:Guanidines / Q000494:pharmacology; D006329:Heart Conduction System / Q000187:drug effects / Q000502:physiology*; D017202:Myocardial Ischemia / Q000175:diagnosis / Q000503:physiopathology*; D010496:Pericardium / Q000502:physiology*; D020110:Pinacidil; D015221:Potassium Channels / Q000187:drug effects / Q000502:physiology*; D013237:Stereoisomerism; D014665:Vasodilator Agents / Q000494:pharmacology
chemical_list: D006146:Guanidines; D015221:Potassium Channels; D014665:Vasodilator Agents; D020110:Pinacidil; D000255:Adenosine Triphosphate; D005905:Glyburide