花生四烯酸对冠心病患者心房肌细胞钠电流的抑制作用

Suppression of sodium current by arachidonic acid in atrial myocytes from patients with coronary heart dis-ease

目的 探讨花生四烯酸对冠心病患者心房肌细胞钠电流的作用。方法 膜片钳全细胞记录技术记录应用花生四烯酸前后人心房肌细胞钠电流。结果 花生四烯酸对人心房肌钠电流的抑制作用表现为电压依赖性和浓度依赖性，ＩＣ５０为１０．３μＭ。用药前后，钠电流的激活曲线几乎重叠，５０％的通道激活点分别为（－４０．８±２．７）ｍＶ和（－４２．５±３．２）ｍＶ（ｎ＝１０，Ｐ＞０．０５）；钠电流失活曲线左移，５０％的通道失活点分别为（－９４．５±３．４）ｍＶ和（－１１６．６±４．ｌ）ｍＶ，即左移（２１．２±３．２）ｍＶ（＝１１，Ｐ＜０．０１）；钠通道失活后恢复时间显著延长，５０％钠通道复活时间分别为（５．９±０．４）ｍｓ和（２７．３±１．７）ｍｓ（ｎ＝８，Ｐ＜０．０１）。结论 花生四烯酸对冠心病患者心房肌细胞钠电流具有抑制和延长复活时间作用。

Objective The aim of this study is to investigate the effect of arachidonic acid (AA)on atrial my- ocytes from patients with coronary heart disease. Methods Patch clamp technique was used to record sodium cur- rent in human atrial myocyte before and after administration of intracellular AA. Results The AA-induced sup- pression on sodium current was voltage-dependent and concentration-dependent, IC50 was 10.3 μM. The activation curves from relative conductances in the absence and presence of 10 μM were almost overlapped. The 50% channel activation points were (-40.8 ± 2.7) mV and (-42.5 ± 3.1) mV respectively (n = 10, P >0.05). AA at 10 μM shifted the steady-state inactivation curve to left from (- 94.5 ± 3.4) mV to( - 116.6 ± 4.1) mV at 50% channel inactivation point (n=11, P <0.01). The 50% recovery time from the inactivation state was significantly slow in the presence of AA at 10μM, that was, from(5.9±0.4)ms to(27.3±1.7)ms(n=8,P<0.01). Conclusion By suppressing sodium current arachidonic acid prolongs the duration of recovery from inactivation in atrial myocytes of patients with coronary heart disease.