Gong Dong-mei, Shan Hong-li, Zhou Yu-hong, Dong De-li, Yang Bao-feng
Department of Pharmacology, Harbin Medical University, Harbin 150086, China.
Yao Xue Xue Bao. 2004 May;39(5):328-32.
To observe the effects of ouabain and aconitine on APD and ion channels in isolated guinea pig and rat ventricular myocytes; to elucidate the action mechanisms of these two drugs and set up new arrhythmic models on cellular level.
In isolated ventricular myocytes of guinea pig and rat, the effects of ouabain and aconitine on APD, ICa-L, Ik, Ito and Ik1 were observed using the whole cell patch clamp technique.
Ouabain (5 micromol x L(-1)) obviously prolonged the APD90, increased ICa-L, decreased Ik and Ik1 in guinea pig ventricular myocytes. Aconitine (1 micromol x L(-1)) lengthened the APD90, increased ICa-L, decreased Ito and increased Ik1 in rat ventricular myocytes.
The targets on ouabain- and aconitine-induced arrhythmias included APD, ICa-L, Ik, Ito, and Ik1. APD, ICaL, Ik and Ito must be the powerful ones, both in arrhythmic and antiarrhythmic courses. The ouabain- and aconitine- induced arrhythmic models on cellular level were built to study the antiarrhythmic mechanisms of chemicals and evaluate new drugs. These two new-type models in vitro were stable, liable, repeatable and economic, which were superior to those typical models in vivo.
观察哇巴因和乌头碱对豚鼠和大鼠离体心室肌细胞动作电位时程（APD）及离子通道的影响；阐明这两种药物的作用机制，并在细胞水平建立新的心律失常模型。
应用全细胞膜片钳技术，观察哇巴因和乌头碱对豚鼠和大鼠离体心室肌细胞APD、L型钙电流（ICa-L）、钾电流（Ik）、瞬时外向钾电流（Ito）和内向整流钾电流（Ik1）的影响。
哇巴因（5 μmol·L⁻¹）可明显延长豚鼠心室肌细胞的APD90，增加ICa-L，降低Ik和Ik1。乌头碱（1 μmol·L⁻¹）可延长大鼠心室肌细胞的APD90，增加ICa-L，降低Ito，增加Ik1。
哇巴因和乌头碱致心律失常的靶点包括APD、ICa-L、Ik、Ito和Ik1。APD、ICa-L、Ik和Ito在心律失常和抗心律失常过程中必定是重要的靶点。建立了哇巴因和乌头碱致细胞水平心律失常模型，用于研究化学药物的抗心律失常机制和评价新药。这两种新型体外模型稳定、可靠、可重复且经济，优于那些典型的体内模型。
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