Lee Young Soo, Chang Po-Cheng, Hsueh Chia-Hsiang, Maruyama Mitsunori, Park Hyung Wook, Rhee Kyoung-Suk, Hsieh Yu-Cheng, Shen Changyu, Weiss James N, Chen Zhenhui, Lin Shien-Fong, Chen Peng-Sheng
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.
J Cardiovasc Electrophysiol. 2013 Oct;24(10):1144-53. doi: 10.1111/jce.12176. Epub 2013 May 29.
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 .
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).
We conclude that IKAS is increased in MI ventricles and contributes significantly to ventricular repolarization especially during tachycardia.
心力衰竭时对蜂毒明肽敏感的小电导钙激活钾电流（IKAS）增加。目前尚不清楚心肌梗死（MI）是否也与IKAS增加有关。
我们对6个正常心脏和10个患有慢性（5周）MI的心脏进行了Langendorff灌注和光学映射。另外6个正常心脏和10个MI心脏用于膜片钳研究。梗死面积为25%（95%置信区间，20 - 31），左心室射血分数为50（46 - 54）。这些兔子没有心力衰竭症状。梗死周边区（PZ）复极化至80%时的动作电位时程（APD80）为150（142 - 159）毫秒，显著（P = 0.01）短于正常心室（167 [158 - 177]毫秒）。PZ的细胞内钙瞬变持续时间也比正常心室短（148 [139 - 157]毫秒）（正常心室为168 [157 - 180]毫秒；P = 0.017）。蜂毒明肽使PZ的APD80延长了9.8（5.5 - 14.1）%，大于正常心室（2.8 [1.3 - 4.3]%，P = 0.006）。在MI心脏快速起搏停止时观察到APD80显著缩短，而正常心室未出现。蜂毒明肽可防止起搏后APD80缩短。膜片钳研究表明，PZ细胞中的IKAS显著高于正常细胞（2.51 [1.55 - 3.47] pA/pF，N = 17）（正常细胞为1.08 [0.36 - 1.80] pA/pF，N = 15，P = 0.019）。
我们得出结论，MI心室中IKAS增加，并且对心室复极化有显著贡献，尤其是在心动过速期间。
