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目的：观察牛磺酸对正常和感染柯萨奇Ｂ３病毒大鼠心肌细胞Ｌ型钙通道的影响．方法：用膜片箝技术记录经Ｌ型钙通道的Ｃａ２＋电流．结果：正常心肌细胞Ｌ型钙通道的Ｃａ２＋电流密度为４１±０８ｐＡ／ｐＦ，柯萨奇Ｂ３病毒感染后Ｃａ２＋电流密度增加到４９±１４ｐＡ／ｐＦ．牛磺酸１６ｍｍｏｌ·Ｌ－１不仅使正常心肌细胞Ｌ型钙通道的Ｃａ２＋电流密度降为３５±０５ｐＡ／ｐＦ，也使感染柯萨奇Ｂ３病毒后心肌细胞的Ｃａ２＋电流密度降为３８±０８ｐＡ／ｐＦ．柯萨奇Ｂ３病毒感染使引起最大Ｃａ２＋电流的膜电压（Ｖｐ）由８±８ｍＶ减为５±３ｍＶ，牛磺酸可使降低的Ｖｐ恢复到８±４ｍＶ．结论：牛磺酸抑制柯萨奇Ｂ３病毒感染引起的Ｃａ２＋电流的增加，并使因感染而降低的引起最大Ｃａ２＋电流的膜电压正常化．牛磺酸对Ｌ型钙通道的影响是牛磺酸减轻病毒感染引起的细胞内Ｃａ２＋增加和异常电活动的机制之一．
Objective: To observe the effect of taurine on L-type calcium channels in normal and infected Coxsackie B3 virus-induced rat cardiomyocytes. Methods: Patch-clamp technique was used to record Ca2 + current through L-type calcium channel. Results: The Ca2 + current density of L-type calcium channel in normal cardiomyocytes was 41 ± 08pA / pF. After Coxsackie B3 infection, the current density of Ca2 + increased to 49 ± 14pA / pF. Taurine 16 mmol·L-1 not only reduced the current density of Ca2 + in L-type calcium channel of normal cardiomyocytes to 3.5 05 pA / pF, but also reduced the current density of Ca2 + in cardiomyocytes infected with coxsackievirus B3 3 8 ± 0 8pA / pF. Coxsackie B3 infection caused a decrease in membrane voltage (Vp) causing maximal Ca2 + currents from 8 ± 8 mV to 5 ± 3 mV, while taurine restored a decreased Vp to 8 ± 4 mV. CONCLUSIONS: Taurine inhibits the increase of Ca2 + currents induced by Coxsackie B3 virus infection and normalizes the membrane voltage resulting from infection that causes the largest Ca2 + currents. The effect of taurine on L-type calcium channels is one of the mechanisms by which taurine attenuates the increase of intracellular Ca2 + and abnormal electrical activity caused by virus infection.