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中文摘要：
目的：探讨二氧化硫（SO2）及其衍生物对心血管系统的作用机制。方法：采用全细胞膜片钳技术研究了茶多酚（TP）对SO2衍生物引起的大鼠心肌细胞钠电流（INa）增大效应的影响。结果：①加入不同浓度的TP（10、20、50mg／L）后，SO2衍生物引起的增大的，。逐渐减小，TP50mg／L时，INa与对照相比无显著差异；②SO2衍生物引起INa激活曲线左移，但并不显著。而加入50mg／LTP后，激活曲线显著恢复；③TP显著影响钠通道的失活过程。SO2衍生物作用前后，半数失活电压（V。）分别为-（71．94±0．23）mV、-（65．79±0．69）mV，n=8，P＜0．01。加入50mg／LTP后，Vh为-（68．64±0．51）mV（n=8），与对照相比无显著差异（P＞0．05），失活曲线的斜率因子未见改变。结论：TP对SO2衍生物引起的心肌细胞k的增大具有抑制作用，提示SO2衍生物对大鼠心肌细胞的毒性作用主要是通过自由基的氧化损伤实现的。
英文摘要：
AIM ： To probe into the toxicological mechanism of sulfur dioxide （ SO2 ） and its derivatives on cardiovascular system. METHODS： Effects of tea polyphenols （TP） on the increase in sodium current （INa） induced by SO2 derivatives in the cardiomyocytes were studied using the whole cell patch - clamp technique. RESULTS ： ① The increase in INa induced by SO2 derivatives was inhibited by treating the cells with TP at different concentrations （ 10, 20 or 50 mg/L） in a dose dependent manner. At concentration of 50 mg/L, TP completely inhibited the increase in INa by SO2 derivatives. ② SO2 derivatives led to shift left of the activation curve. After application of TP at dose of 50 mg/L, the curve showed resumed significantly. ③ TP changed the inactivation process significantly. Before and after the application of SO2 derivatives, the half- inactivation voltage of INa was - （71.94 ± 0. 23 ） mV and - （65.79 ± 0. 69） mV （ n = 8, P 〈 0. 01 ）. However, after the application of TP, the half- inactivation voltage was - （68.64 ± 0. 51 ） mV （n = 8 ）, without changing the slope factor, but it was not significant compared with the control （ P 〉 0.05 ）. CONCLUSION ： TP inhibits the incremental effects of SO2 derivatives on INa, suggesting that the toxicity of SO2 on cardiomyoeytes of rat is induced by free radical.
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