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Apamin‐Sensitive Calcium‐Activated Potassium Currents in Rabbit Ventricles with Chronic Myocardial Infarction
Author(s) -
LEE YOUNG SOO,
CHANG POCHENG,
HSUEH CHIAHSIANG,
MARUYAMA MITSUNORI,
PARK HYUNG WOOK,
RHEE KYOUNGSUK,
HSIEH YUCHENG,
SHEN CHANGYU,
WEISS JAMES N.,
CHEN ZHENHUI,
LIN SHIENFONG,
CHEN PENGSHENG
Publication year - 2013
Publication title -
journal of cardiovascular electrophysiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.193
H-Index - 138
eISSN - 1540-8167
pISSN - 1045-3873
DOI - 10.1111/jce.12176
Subject(s) - medicine , apamin , cardiology , repolarization , myocardial infarction , left ventricles , optical mapping , perfusion , calcium , electrophysiology , ventricle
SK Currents in Chronic MI Introduction The apamin‐sensitive small‐conductance calcium‐activated potassium current (I KAS ) is increased in heart failure. It is unknown if myocardial infarction (MI) is also associated with an increase of I KAS . Methods and 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 (APD 80 ) 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 APD 80 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 APD 80 was observed at the cessation of rapid pacing in MI but not in normal ventricles. Apamin prevented postpacing APD 80 shortening. Patch clamp studies showed that I KAS 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). Conclusion We conclude that I KAS is increased in MI ventricles and contributes significantly to ventricular repolarization especially during tachycardia.