首页> 外文会议>2010 Computers in Cardiology >Beta-adrenergic modulation of heart rate: Contribution of the slow delayed rectifier K+ current (IKs)
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Beta-adrenergic modulation of heart rate: Contribution of the slow delayed rectifier K+ current (IKs)

机译:β-肾上腺素对心率的调节:慢延迟整流器K + 电流(I Ks )的贡献

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To assess the role of the slow delayed rectifier potassium current (IKs) in the β-adrenergic modulation of heart rate, we experimentally determined the effect of β adrenergic stimulation on IKs and used the thus obtained data in computer simulations of SA nodal pacemaker activity, employing the mathematical model of a primary rabbit SA node pacemaker cell by Kurata and coworkers. Incorporation of our experimental findings into the SA nodal cell model resulted in a 12 ms decrease in cycle length. This decrease in cycle length is similar to the 13 ms decrease observed upon incorporation of our experimental data on the effect of β-adrenergic stimulation on the hyperpolarization-activated funny current'' (If), also known as ''pacemaker current''. We conclude that IKs is an important contributor to the β-adrenergic modulation of heart rate.
机译:为了评估慢延迟整流器钾电流(I Ks )在心率的β-肾上腺素调节中的作用,我们通过实验确定了β肾上腺素刺激对I Ks 并将由此获得的数据用于SA节点起搏器活动的计算机模拟中,采用Kurata和同事的主要兔SA结节起搏器细胞的数学模型。将我们的实验结果纳入SA淋巴结细胞模型后,周期长度减少了12 ms。周期长度的减少类似于结合我们关于β-肾上腺素刺激对超极化激活的滑稽电流(I f )的影响的实验数据观察到的13毫秒减少''作为“起搏者潮流”。我们得出的结论是,IKs是心率的β-肾上腺素能调节的重要贡献者。

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