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首页> 外文期刊>Journal of biomedical science. >The vicissitudes of the pacemaker current IKdd of cardiac Purkinje fibers
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The vicissitudes of the pacemaker current IKdd of cardiac Purkinje fibers

机译:心脏浦肯野纤维起搏器电流IKdd的变迁

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The pacemaker potential in cardiac Purkinje fibers has been attributed to the decay of the potassium current IKdd . An alternative proposal is that the hyperpolarization-activated current If underlies the pacemaker potential in all cardiac pacemakers . The aim of this review is to retrace the experimental development related to the pacemaker mechanism in Purkinje fibers with reference to findings about the pacemaker mechanism in the sinoatrial node. Major experimental data were attributed to K + depletion in narrow extracellular spaces which would result in a time-dependent decay of the inward rectifier current IK1. In order to avoid such a postulated depletion, Ba~(2+) was used to block the decay of IK1. However, Ba2 + had also blocked IKdd (and not only IK1). In single Purkinje cells in the absence of Ba2 +, IKdd was present in the pacemaker potential range and reversed at EK. In the presence of Ba2 +, IKdd was blocked and If appeared at potentials negative to the pacemaker range . The pacemaker potential behaves in a manner consistent with the underlying IKdd but not with If. It is concluded that the large boy of evidence supports the pacemaker role of IKdd (but not of If) in Purkinje fibers
机译:心脏浦肯野纤维中起搏器的潜力归因于钾电流IKdd的衰减。另一种建议是,超极化激活电流If是所有心脏起搏器中起搏器电位的基础。这篇综述的目的是参考有关窦房结中起搏器机制的发现,追溯浦肯野纤维中与起搏器机制有关的实验发展。主要的实验数据归因于狭窄的细胞外空间中的K +耗尽,这将导致内向整流器电流IK1随时间的衰减。为了避免这种假定的耗尽,Ba〜(2+)被用来阻止IK1的衰减。但是,Ba2 +也阻止了IKdd(而不仅仅是IK1)。在不存在Ba2 +的单个Purkinje细胞中,IKdd存在于起搏器电势范围内,并在EK处逆转。在Ba2 +存在下,IKdd被阻滞,If出现对起搏器范围负电势。起搏器电位的行为与基础IKdd一致,但与If不一致。结论是,大量证据支持浦肯野纤维中IKdd(而非If)的起搏器作用

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