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目的研究大环内酯类抗生素红霉素对心脏快反应动作电位的影响,初步探讨其诱发心律失常的机制。方法应用细胞内微电极技术,研究红霉素对心肌细胞快反应动作电位的影响;利用钾通道特异性阻断剂chromonal 293B和dofetilide研究红霉素对延迟整流钾电流Ikr和Iks的影响。结果红霉素可使豚鼠心室乳头肌快反应动作电位时程和有效不应期延长,0期最大除极速率降低;在chromanol 293B作用基础上,红霉素仍可显著延长动作电位时程;在应用dofetilide完全阻断Ikr的基础上,观察到它并不延长动作电位时程。结论根据红霉素对动物心脏电生理活动的影响,初步推测其可能通过抑制钠和钾离子通道,而且是通过特异性阻断Ikr而产生诱发心律失常效应。
Objective To study the effect of the macrolide antibiotic erythromycin on the fast acting action potential of heart and to explore the mechanism of its inducing arrhythmia. Methods The intracellular microelectrode technique was used to study the effect of erythromycin on the action potential of cardiomyocytes. The effects of erythromycin on Ikr and Iks of delayed rectifier potassium currents were investigated by potassium channel-specific blockers chromonal 293B and dofetilide. Results Erythromycin could rapidly induce the action potential duration and effective refractory period of guinea pig ventricular papillary muscle, and the maximum depolarization rate of stage 0 decreased. On the basis of chromanol 293B, erythromycin could prolong the action potential duration significantly. Based on the complete blocking of Ikr with dofetilide, it was observed that it did not prolong the action potential duration. Conclusion According to the effect of erythromycin on the electrophysiological activity of the animal heart, it is preliminarily supposed that it may induce the arrhythmic effect by inhibiting the sodium and potassium channels and specifically blocking the Ikr.