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首页> 外文会议>Annual Scientific Conference of Computers in Cardiology >Effects of a Persistent Sodium Current Through Mutated hNav1.5 Sodium Channels on Intracellular Ionic Homeostasis in a Ventricular Cell Model
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Effects of a Persistent Sodium Current Through Mutated hNav1.5 Sodium Channels on Intracellular Ionic Homeostasis in a Ventricular Cell Model

机译：静态钠电流通过突变的HNAV1.5钠通道对心室细胞模型细胞内离子稳态的影响

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In LQT3 patients, SCN5A mutations were found that lead to a small fraction of persistent hNav1.5 current. We explored the effects of such a change on the intracellular ionic homeostasis in a model of guinea-pig cardiac ventricular cell. At steady-state under 1 Hz stimulation, the presence of a persistent Na{sup}+ current (I{sub}(Nap)) with g{sub}(Nap) 0.02 ms/cm{sup}2 led to a prolongation of the action potential from 153 ms (control) to 223 ms and an increase of [Na{sup}+]{sub}i, diastolic and systolic [Ca{sup}(2+)]{sub}i and [Ca{sup}(2+)]{sub}(SRup) by 10%, 30%, 40% and 43%, respectively. These changes were larger at 3 Hz. Such intracellular Na{sup}+ and Ca{sup}(2+) overload was not found when the action potential prolongation (to 222 ms at 1 Hz) was due to decreased I{sub}(Kr) and I{sub}(Ks) currents. The model with I{sub}(Nap) became arrhythmogenic when [K{sup}+]{sub}e was lowered from 5.4 to 5.0 mM, whereas control and low K{sup}+ current models did not produce arrhythmias even when [K{sup}+]{sub}e was 2.5 mM.
机译：在LQT3患者中，发现SCN5A突变，导致持续的HNAV1.5电流的一小部分。我们探讨了这种改变对豚鼠心室细胞模型中细胞内离子稳态的影响。在1 Hz刺激下的稳态，具有G {Sub}（NAP）0.02ms / cm {sup} 2的持久性Na {sup} +电流（i {sub}（nap））的存在导致了延长从153ms（控制）到223ms的动作电位和增加[Na {sup} +] {sub} i，舒张和收缩率[ca {sup}（2 +）] {sub} i和[ca {sup }（2 +）] {sub}（srup）分别为10％，30％，40％和43％。这些变化在3 Hz较大。当动作电位延长（在1 Hz的222毫秒到222ms）是由于I {sub}（kr）和i {sub}时，找不到这种细胞内Na {sup} +和ca {sup}（2+）过载。 KS）电流。当[k {sup} +] {sub} e从5.4降至5.0 mm时，具有I {sub}（nap）的模型变得心血发生，而控制和低k {sup} +当前模型也没有产生心律失常，即使[ k {sup} +] {sub} e为2.5 mm。

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