中文摘要：

目的探讨α1肾上腺素受体在调控快激活延迟整流钾电流（Ikr）中的作用。方法制备豚鼠心肌细胞，采用全细胞膜片钳技术记录心肌细胞Ikr。心肌细胞采用α1肾上腺素受体激动剂苯肾上腺素0．1μmol／L处理后分为五组：A组作为对照；B1、B2、B3和B4组分别以α1肾上腺素受体阻滞剂哌唑嗪1μmol／L棚肾上腺素受体α1A亚型阻滞剂5-甲基乌拉地尔1μmol／L、α1-肾上腺素受体a，B亚型阻滞剂氯乙基可乐定10μmol／L和α1肾上腺素受体α1D亚型阻滞剂BMY-73781nmol／L干预，比较干预前后心肌细胞Ikr的变化。结果B1组和B2组心肌细胞Ikr降为干预前的0．92±0．07和0．97±0．04，高于A组的0．67±0．03（P〈0．01），而B3和B4组心肌细胞Ikr降为干预前的0．64±0．06和0．73±0．07，与A组相仿（P〉0．05）。结论α1肾上腺素受体激活可降低心肌细胞Ikr；该作用主要通过α1肾上腺素受体和α1A亚型介导。

英文摘要：

Objective To explore the effects of α1-adrenergic receptor on regulation of the rapid activation of delayed rectifier potassium current（Ikr）. Methods Guinea pig ventricular myocytes were prepared. Ikr was recorded by whole-cell patch-clamp technique. Myocardial cells were treated with 0. 1μmol/L α1 epinephrine agonist phenylephrine, which were assigned into 5 groups of A（control）, B1 （intervened withal adrenaline receptor blocker prazosin 1μmol/L, 132 （intervened withα1A adrenaline receptor blocker 5-methylurapidil 1 μmol/L）, 133 （intervened with alB adrenaline receptor blocker cholorethylclonidine 10 μmol/L） and B4（intervened with α1D adrenaline receptor blocker BMY-7378 1 nmol/L）. The value of Ikr was compared before and after intervention. Results After treatment, the values of Iuwere decreased to 0.92±0. 07 and 0. 97!0. 04 of before in groups of B1 and 132,which were higher than 0. 67±0. 03 in group A（P〈0. 01）. The decreases of Iuafter intervention in groups of 133 and B4（0. 64±0. 06 and 0. 73±0. 07） were not significantly different from those in group A （P〈0. 05）. Conclusion The activation of α1-adrenergic receptor can reduce Ikr of myocardial cells, which is mainly mediated via alA-adrenergic receptor.