Electrophysiologic characteristics of atrial myocytes in levo-thyroxine-treated rats.
Electrophysiologic characteristics of atrial myocytes in levo-thyroxine-treated rats.
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DOI：
10.1089/thy.2005.15.3
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发表时间：
2005-02
期刊：
影响因子：
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通讯作者：
M. Sunagawa;Munesada Yamakawa;M. Shimabukuro;N. Higa;N. Takasu;T. Kosugi
中科院分区：
文献类型：
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作者：
M. Sunagawa;Munesada Yamakawa;M. Shimabukuro;N. Higa;N. Takasu;T. Kosugi
为了研究甲状腺激素是否调节心房肌细胞的电特性，测量了心电图（ECG）、动作电位（AP）和离子电流。雄性Sprague-Dawley大鼠在6周龄时随机分为对照组和左旋甲状腺素（T4）治疗组。每天将左旋甲状腺素（500 μ g/kg体重）注射到腹膜腔中，持续14天（T4治疗大鼠），每天将相同体积的生理盐水注射到对照大鼠中。使用心尖-基底导联记录ECG信号。采用膜片钳技术检测AP、电压依赖性Na+和L型Ca 2+通道电流（I（Na）和I（Ca（L）、内向整流K+通道电流（I（K1））、瞬时外向K+通道电流（I（to））和延迟整流K+通道电流（I（K（delay）。T4处理显著改变了大鼠心房肌细胞的电特性，包括（1）心率增加，（2）细胞大小增加，（3）动作电位时程（APD）缩短，（4）细胞膜电容（C（m））增加，（5）输入电阻（R（in））降低。虽然T4处理的心房肌细胞的I（Na）和I（K1）的电流密度与对照细胞的电流密度没有差异，但T4处理的大鼠的I（Ca（L））显著降低，I（K（延迟））显著增加。因此，甲状腺毒症可通过改变心房肌细胞I（Ca（L））和I（K（delay））的电流密度而引起APD缩短。
To investigate whether thyroid hormone modulates electrical properties of atrial myocytes, electrocardiogram (ECG), action potentials (APs), and ionic currents were measured. Male Sprague-Dawley rats were randomly divided into control and levo-thyroxine (T4)-treated groups at 6 weeks of age. Levo-thyroxine (500 microg/kg of body weight) was injected daily into the peritoneal cavity for 14 days (T4-treated rats) and the same volume of saline was injected in control rats daily. ECG signals were recorded using apex-base leads. APs, voltage-dependent Na+ and L-type Ca2+ channel current (I(Na) and I(Ca(L))), inwardly rectifying K+ channel current (I(K1)), transient outward K+ channel current (I(to)), and delayed rectifier K+ channel current (I(K(delay))) were measured using patch-clamp techniques. T4 treatment significantly changed electrical properties in rat atrial myocytes, including (1) the increase in heart rate, (2) the increase in cell size, (3) the shortening of action potential duration (APD), (4) the increase in cell membrane capacitance (C(m)), and (5) the decrease in input resistance (R(in)). Although the current densities of I(Na) and I(K1) in T4-treated atrial myocytes did not differ from those in control cells, I(Ca(L)) was significantly decreased and I(K(delay)) was significantly increased in T4-treated rats. Thus, thyrotoxicosis could induce the shortening of APD by alterations in current density of both I(Ca(L)) and I(K(delay)) in rat atrial myocytes.