目的 研究康普瑞汀磷酸二钠（CA4P）对豚鼠心室肌细胞动作电位间期（APD）和人类ether-a-go-go相关基因（hERG）编码的K⁺离子通道的影响，探讨CA4P对心脏毒性作用的体外细胞学机制。方法 使用全细胞膜片钳技术记录CA4P 10、100 μmol/L作用下豚鼠心肌细胞的动作电位，并记录CA4P 3、10、30、100、300 μmol/L下对HEK293细胞hERG通道尾电流的抑制率及CA4P 30 μmol/L在10、20、30、40、50 mV时对hERG电流的抑制率。结果 CA4P 10、100 μmol/L显著延长动作电位复极50%时程（ADP₅₀）和动作电位复极90%时程（ADP₉₀）。CA4P可浓度相关性和电压相关性抑制hERG尾电流幅度，半数抑制浓度（IC₅₀）为54.9 μmol/L，安全边缘范围为30.5～2.8。结论 CA4P可延长动作电位间期及抑制hERG通道电流。

Objective To investigate the effects of combretastatin A4 phosphate (CA4P) on action potential duration (APD) and human-ether-a-go-go-related gene (hERG) K⁺ channel of ventricle muscle cell in cavy, and to explore in vitro celluar mechanism of CA4P in cardiotoxicity effects.Methods APD of ventricle muscle cell in cavy under the action of CA4P 10 and 100 μmol/L were recorded by the whole cell patch clamp technique. The inhibition ratio of hERG channel tail current under the action of CA4P 3, 10, 30, 100, and 300 μmol/L and the inhibition ratio of hERG channel tail current under the action of CA4P 30 μmol/L in 10, 20, 30, 40, and 50 mV were recorded. Results CA4P 10 and 100 μmol/L significantly prolonged the action potential duration at 50% of repolarization (ADP₅₀) and the action potential duration at 90% of repolarization (ADP₉₀). CA4P induced a concentration- and voltage-dependent inhibition of the current amplitude in the hERG tail current. The half-maximal inhibitory concentration (IC₅₀) was 54.9 μmol/L. The safety margin ratio was 30.5-2.8. Conclusion CA4P can prolong APD and inhibit hERG channel current.