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目的:研究1-(2,6-二甲基苯氧基)-2-(3,4-二甲氧基苯乙氨基)丙烷盐酸盐(DDPH)对豚鼠心室肌细胞快激活(I_(Kr))和慢激活(I_(Ks))延迟整流钾电流的作用.方法:全细胞膜片箝技术.结果:DDPH 0.1-100μmol/L浓度依赖性抑制I_(Kr),I_Kr-tail[IC_(50)(μmol/L)为6.1,95％可信限为(2.8—13.5)].DDPH同时浓度依赖性抑制 I_(Ks),I_(Ks-tail[IC_(50)(μmol/L)为12.5,95％可信限为(4.8-32.2)].DDPH(10 μmol/L)不影响I_(Kr)和I_(Ks)的电压依赖性激活过程,给药前I_(Kr)的半激活电压(V_(1/2),mV)和斜率因子(k,mV)分别为(-21.7±0.8)和(5.9±0.8),给药后分别为(-23.5±2.4)和(8.1±2.2),无统计学意义(P>0.05).用药前后I_(Ks)的半激活电压和斜率因子的差异亦无统计学意义(P>0.05),用药前分别为(27.0±0.8)和(14.9± 0.9),用药后分别为(27.1±0.7)和(16.6±0.8).DDPH(<10μmol/L)可抑制 I_(Kr)和 I_(Ks)的去激活过程,并且加快I_(Kr)的失活.结论:DDPH抑制I_(Kr)和I_(Ks)无选择性.且主要作用于其去激活过程,而非激活过程.DDPH进一步通过加速其失活过程抑制I_(Kr).
AIM: To investigate the effects of 1- (2,6-dimethylphenoxy) -2- (3,4-dimethoxyphenethylamino) propane hydrochloride (DDPH) on the activation of guinea pig ventricular myocytes (Ks) and delayed activation (I_ (Ks)) .Methods: The whole cell patch clamp technique was used.Results: DDPH 0.1-100μmol / L inhibited I Kr and I Kr tail in a concentration- 50 μmol / L was 6.1 and the 95% confidence interval was 2.8-13.5.] DDPH inhibited I_ (Ks) and I_ (Ks-tail [IC_ (50) 12.5, 95% confidence interval (4.8-32.2)]. DDPH (10 μmol / L) did not affect the voltage-dependent activation of I Kr and I Ks, The voltages (V_ (1/2), mV) and the slope factor (k, mV) were -21.7 ± 0.8 and 5.9 ± 0.8, respectively, and were (-23.5 ± 2.4) and ), There was no statistical significance (P> 0.05) .There was no significant difference in half activation voltage and slope factor of I_ (Ks) before and after treatment (P> 0.05) ± 0. 9), respectively, and (27.1 ± 0.7) and (16.6 ± 0.8) dDPH (<10μmol / L) inhibited the deactivation of I Kr and I Ks, Inactivation.Conclusion: DDPH inhibits I_ (Kr) and I_ (Ks) To act on its deactivation process, but not the activation process.DDPH further inhibits I_ (Kr) by accelerating its inactivation process.