Nie Aifang, Meng Ziqiang
Institute of Environmental Medicine and Toxicology, Shanxi University, Taiyuan 030006, China.
Biochim Biophys Acta. 2005 Dec 10;1718(1-2):67-73. doi: 10.1016/j.bbamem.2005.09.020. Epub 2005 Oct 21.
The effects of sulfur dioxide (SO(2)) derivatives (bisulfite and sulfite, 1:3 M/M) on voltage-dependent sodium channel in isolated rat ventricular myocyte were studied using the whole cell patch-clamp technique. SO(2) derivatives increased sodium current (I(Na)) in a concentration-dependent manner. SO(2) derivatives at 10 microM significantly shifted steady-state inactivation curve of I(Na) to more positive potentials, but did not affect the activation curve. SO(2) derivatives markedly shifted the curve of time-dependent recovery of I(Na) from inactivation to the left, and accelerated the recovery of I(Na). SO(2) derivatives also significantly shortened the activation and inactivation time constants of I(Na). These results indicated that SO(2) derivatives produced concentration-dependent stimulation of cardiac sodium channels, which due mainly to the interaction of the drug with sodium channels in the inactivated state.
采用全细胞膜片钳技术研究了二氧化硫（SO₂）衍生物（亚硫酸氢盐和亚硫酸盐，摩尔比1:3）对离体大鼠心室肌细胞电压依赖性钠通道的影响。SO₂衍生物以浓度依赖性方式增加钠电流（I(Na)）。10微摩尔的SO₂衍生物使I(Na)的稳态失活曲线显著向更正电位移动，但不影响激活曲线。SO₂衍生物使I(Na)从失活状态的时间依赖性恢复曲线明显向左移动，并加速了I(Na)的恢复。SO₂衍生物还显著缩短了I(Na)的激活和失活时间常数。这些结果表明，SO₂衍生物对心脏钠通道产生浓度依赖性刺激，这主要是由于药物与失活状态的钠通道相互作用所致。
