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应用膜片钳全细胞记录技术研究青藤碱 (Sin)对酶解分离的豚鼠单个心室肌细胞膜钠离子电流 (INa)、L型钙电流 (ICa L)的影响。发现 1,5 ,10 μmol/L的Sin分别使INa峰值 (INamax)较用药前下降 2 3.2 %、36 .1%和 6 0 % (n =8,P均 <0 .0 5 ) ;使ICa L峰值 (ICa Lmax)较用药前下降了 12 .8% ,35 .9%和 46 .9% (n =8,P均 <0 .0 1)。Sin使INa及ICa L电流 电压曲线上移 ,但不使其峰值电位偏移。Sin还浓度依赖性减慢钠通道灭活后恢复过程。当刺激频率分别为 0 .5 ,1,2Hz时 ,5 μmol/LSin使INamax较用药前分别下降了 36 .1%、41.5 %和 48.0 % (n =8,P均 <0 .0 1)。结果表明 ,Sin对INa具浓度和频率依赖性阻滞作用 ,可能作用于其失活状态 ;Sin对ICa L具浓度依赖性阻滞作用。这可能为其抗心律失常的重要机制。
The effects of sinomenine on sodium current (INa) and L-type calcium current (ICa L) in isolated guinea pig ventricular myocytes were studied using patch-clamp whole cell recording technique. The results showed that the INmax of INa was decreased by 3.2%, 36.1% and 60%, respectively (P = <0.55), and the peak values of ICa ICa Lmax decreased by 12.8%, 35.9% and 46.9% (n = 8, P <0.01) before treatment. Sin shifts the current and voltage curves INa and ICa L up without shifting their peak potentials. Sin also slows down the sodium channel inactivation recovery in a concentration-dependent manner. When the stimulation frequency was 0 .5, 1 and 2 Hz respectively, 5 μmol / LSin decreased INamax by 36.1%, 41.5% and 48.0%, respectively (n = 8, P <0.01). The results showed that Sin had a concentration-dependent and frequency-dependent block on INa, which might be at its inactivation state. Sin inhibited the ICa L in a concentration-dependent manner. This may be its anti-arrhythmic important mechanism.