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中文摘要：
目的探讨正常和持续性心房颤动时犬心房肌M3受体介导IKM3电流的变化及苦参碱对IKM3的作用，为筛选抗心律失常药物作用靶点提供理论和实验依据。方法建立快速心房起搏致心房颤动犬模型，通过膜片钳技术比较犬心房肌正常和模型组电流变化及药物作用的不同。结果持续性心房颤动犬心房肌IKM3电流密度明显增高（实验电压＋50mV时，232±81pAvs198±80pA，n=4，P〈0．05），苦参碱对IKM3电流有抑制作用，且对正常组抑制作用明显高于模型组。结论M3受体及其介导的IKM3电流可能是治疗房颤的新靶点。
英文摘要：
Aim To investigate changes of M3 receptormediated delayed rectifier K current （IKM3） in atrial myocytes of canine models with persistent atrial fibrillation （AF） and normal dogs, and the effects of matrine on IKM3 to provide theoretical and experimental evidences for new target of drug therapy. Methods AF models were established through rapid pacing. Wholecell patch technique was used to record the current changes of atrial myocytes isolated from normal and AF model dogs and the drug effects were compared. Resuits IKM3 density was significantly increased （232 ±81 pA, n = 4） in canine atrial myocytes from persistent AF models Compared with normal dogs（ 198 ± 80 pA,n = 4 ） at test potential of ＋ 50 mV. The inhibitory effect of matrine on IKM3 was more potent in normal dogs than in AF model dogs. Conclusion M3 receptor-mediated delayed rectifier K current （IKM3）might be the new therapeutic target in future AF treatment.
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