title: Apamin-sensitive calcium-activated potassium currents in rabbit ventricles with chronic myocardial infarction.
abstract: BACKGROUND
  The apamin-sensitive small-conductance calcium-activated potassium current (IKAS ) is increased in heart failure. It is unknown if myocardial infarction (MI) is also associated with an increase of IKAS .
  
  
  RESULTS
  We performed Langendorff perfusion and optical mapping in 6 normal hearts and 10 hearts with chronic (5 weeks) MI. An additional 6 normal and 10 MI hearts were used for patch clamp studies. The infarct size was 25% (95% confidence interval, 20-31) and the left ventricular ejection fraction was 50 (46-54). The rabbits did not have symptoms of heart failure. The action potential duration measured to 80% repolarization (APD80 ) in the peri-infarct zone (PZ) was 150 (142-159) milliseconds, significantly (P = 0.01) shorter than that in the normal ventricles (167 [158-177] milliseconds. The intracellular Ca transient duration was also shorter in the PZ (148 [139-157] milliseconds) than that in normal ventricles (168 [157-180] milliseconds; P = 0.017). Apamin prolonged the APD80 in PZ by 9.8 (5.5-14.1)%, which is greater than that in normal ventricles (2.8 [1.3-4.3]%, P = 0.006). Significant shortening of APD80 was observed at the cessation of rapid pacing in MI but not in normal ventricles. Apamin prevented postpacing APD80 shortening. Patch clamp studies showed that IKAS was significantly higher in the PZ cells (2.51 [1.55-3.47] pA/pF, N = 17) than in the normal cells (1.08 [0.36-1.80] pA/pF, N = 15, P = 0.019).
  
  
  CONCLUSIONS
  We conclude that IKAS is increased in MI ventricles and contributes significantly to ventricular repolarization especially during tachycardia.
authors.affiliation: Krannert Institute of Cardiology and Division of Cardiology, Department of Medicine, Indianapolis, Indiana, USA; Division of Cardiology, Department of Internal Medicine, Catholic University of Daegu School of Medicine, Daegu, Korea.
authors.forename: Young Soo
authors.initials: YS
authors.lastname: Lee
authors.forename: Po-Cheng
authors.initials: PC
authors.lastname: Chang
authors.forename: Chia-Hsiang
authors.initials: CH
authors.lastname: Hsueh
authors.forename: Mitsunori
authors.initials: M
authors.lastname: Maruyama
authors.forename: Hyung Wook
authors.initials: HW
authors.lastname: Park
authors.forename: Kyoung-Suk
authors.initials: KS
authors.lastname: Rhee
authors.forename: Yu-Cheng
authors.initials: YC
authors.lastname: Hsieh
authors.forename: Changyu
authors.initials: C
authors.lastname: Shen
authors.forename: James N
authors.initials: JN
authors.lastname: Weiss
authors.forename: Zhenhui
authors.initials: Z
authors.lastname: Chen
authors.forename: Shien-Fong
authors.initials: SF
authors.lastname: Lin
authors.forename: Peng-Sheng
authors.initials: PS
authors.lastname: Chen
mesh_terms: D000200:Action Potentials; D000818:Animals; D001030:Apamin / Q000494:pharmacology*; D002304:Cardiac Pacing, Artificial; D002908:Chronic Disease; D004195:Disease Models, Animal; D004562:Electrocardiography; D005260:Female; D006339:Heart Rate; D066298:In Vitro Techniques; D007700:Kinetics; D009203:Myocardial Infarction / Q000378:metabolism* / Q000473:pathology / Q000503:physiopathology; D009206:Myocardium / Q000378:metabolism* / Q000473:pathology; D018408:Patch-Clamp Techniques; D010477:Perfusion; D011188:Potassium / Q000378:metabolism*; D026902:Potassium Channel Blockers / Q000494:pharmacology*; D024681:Potassium Channels, Calcium-Activated / Q000037:antagonists & inhibitors* / Q000378:metabolism*; D011817:Rabbits; D013318:Stroke Volume; D013610:Tachycardia / Q000378:metabolism / Q000503:physiopathology; D016277:Ventricular Function, Left
chemical_list: D026902:Potassium Channel Blockers; D024681:Potassium Channels, Calcium-Activated; D001030:Apamin; D011188:Potassium
keywords: action potentials; intracellular calcium; ion channels; myocardial infarction; potassium currents; repolarization reserve