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目的：探讨青蒿素抗心律失常的离子电流基础。方法：用全细胞膜片钳技术和双电极电压钳技术。结果：当细胞超极化到－１００ｍＶ时，青蒿素以浓度依赖方式明显抑制家兔心室肌细胞Ｉｋ１，５０μｍｏｌ·Ｌ－１青蒿素可使家兔心室肌细胞Ｉｋ１从对照组的－２３６±０３９ｎＡ减少到－１４３±０３１ｎＡ。给予非洲蛙卵母细胞注射Ｋｉｒ２．１ｃＲＮＡ后，用不同浓度青蒿素灌注，可减低Ｋｉｒ２．１钾通道电流，此作用呈电压和浓度依赖性。青蒿素对Ｋｉｒ２．１钾通道的阻断作用呈可逆性。结论：青蒿素能有效抑制离体心肌细胞Ｉｋ１，其抗心律失常作用机理与其抑制心肌细胞Ｉｋ１及阻断Ｋｉｒ２．１通道电流有关。
Objective: To study the basic current of artemisinin antiarrhythmic ion current. Methods: Whole-cell patch-clamp technique and bipolar voltage clamp technique. RESULTS: Artemisinin significantly inhibited Ik1 in rabbit ventricular myocytes in a dose-dependent manner when artemisinin was hyperpolarized to -100 mV and decreased the Ik1 level in rabbit ventricular myocytes from 2 36 ± 0.39 nA reduced to -1 43 ± 0 31nA. After injecting Kir2.1cRNA into African frog oocytes, the currents of Kir2.1 potassium channel can be reduced by different concentrations of artemisinin, and the effect is voltage and concentration dependent. The blocking effect of artemisinin on Kir2.1 potassium channel was reversible. Conclusion: Artemisinin can effectively inhibit Ik1 in vitro and its anti-arrhythmic mechanism is related to inhibiting Ik1 and blocking Kir2.1 channel current.