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为探讨四氢巴马汀（ＴＨＰ）抗心律失常作用的离子机制，我们采用膜片钳技术观察了ＴＨＰ对豚鼠心室肌单细胞外向钾电流及尾电流的影响。当保持电压－４０ｍＶ，指令电压６０ｍＶ时，心室肌细胞延迟外向钾电流和尾电流最大。灌流含ＴＨＰ１０μｍｏｌ／Ｌ的台氏液后，延迟外向钾电流和尾电流显著下降。在指令电压－２０ｍＶ时，尾电流可从（４８．６±１０．５）ｐＡ降至（３３．３±１１．２）ｐＡ，指令电压５０ｍＶ时尾电流从（９４．５±１９．３）ｐＡ降至（５８．５±２０．５）ｐＡ．在指令电压５０ｍＶ时延迟外向钾电流也从（３６２．８±７６）ｐＡ下降到（１３４．６±３６．７）ｐＡ，上述变化在以台氏液冲洗２０ｍｉｎ后恢复至原来水平。实验结果表明，ＴＨＰ抗心律失常作用与其抑制延迟外向钾电流和尾电流有关。
To investigate the ionic mechanism of anti-arrhythmic action of tetrahydropalmatine (THP), we used patch-clamp technique to observe the effect of THP on single cell outward potassium currents and tail currents in guinea pig ventricular myocytes. When holding voltage -40mV, command voltage 60mV, ventricular myocytes delayed outward potassium current and tail current maximum. After perfusion with Tyrode’s solution containing THP10μmol / L, the outward potassium currents and tail currents were delayed significantly. The tail current can be reduced from (48.6 ± 10.5) pA to (33.3 ± 11.2) pA at command voltage of -20mV and from (94.5 ± 19.3) at command voltage of 50mV. pA decreased to (58.5 ± 20.5) pA. Delayed outward potassium current also dropped from (362.8 ± 76) pA to (134.6 ± 36.7) pA at a command voltage of 50 mV, and the changes recovered to their original level after rinsing with Tyrode’s solution for 20 min. The experimental results show that, THP anti-arrhythmic effect and its inhibition of delayed outward potassium current and tail current.