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The intracellular sodium activity of sheep heart Purkinje fibres: effects of local anaesthetics and tetrodotoxin

机译:绵羊心脏浦肯野纤维的细胞内钠活性:局部麻醉药和河豚毒素的影响

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摘要

1. The intracellular Na activity (aNai) of quiescent sheep heart Purkinje fibres has been measured using Na+-sensitive glass micro-electrodes. The effects of local anaesthetics (procaine and lidocaine) and tetrodotoxin (TTX) have been investigated.2. Local anaesthetics reduced the steady-state level of the intracellular Na activity in a dose-dependent manner. The highest concentrations used (10-2 M) reduced the intracellular Na activity by about 25%.3. TTX decreased the steady-state level of the intracellular Na activity. At a concentration of 10-6 g/ml. (3·13 × 10-6 M), TTX produced a decrease in intracellular Na activity of approximately 10%.4. The initial rate of rise of the intracellular Na activity upon addition of the cardioactive steroid strophanthidin (10-5 M) was used to estimate the net passive Na influx.5. Procaine (5 × 10-4 M) caused a 50% reduction of this rate of rise of the intracellular Na activity. The highest concentration of procaine used (10-2 M) decreased the rate of rise by approximately 80%.6. Procaine (5 × 10-3 M) also reduced the rate of rise of intracellular Na produced by the removal of external K (Ko), and prevented the large depolarization associated with the absence of Ko.7. TTX also produced a decrease in the rate of rise of the intracellular Na activity that occurs upon addition of strophanthidin. A maximum effect was produced in our experiments at a TTX concentration of 10-6 g/ml. At this concentration the rate of rise of intracellular Na activity was reduced by approximately 40% at a membrane potential of -70 mV.8. We conclude from our experiments that the effects of local anaesthetics and TTX on the intracellular Na activity are brought about by a reduction of the Na permeability of the cell membrane, and that at the normal resting potential, Na entry through TTX-sensitive channels contributes greatly to the total net Na influx.
机译:1.使用Na + 敏感的玻璃微电极测量了静态绵羊心浦肯野纤维的细胞内Na活性(aNa i )。研究了局部麻醉药(普鲁卡因和利多卡因)和河豚毒素(TTX)的作用。2。局部麻醉剂以剂量依赖的方式降低了细胞内Na活性的稳态水平。最高浓度(10 -2 M)使细胞内Na活性降低了约25%。3。 TTX降低了细胞内Na活性的稳态水平。浓度为10 -6 g / ml。 (3·13×10 -6 M),TTX使细胞内Na活性降低约10%.4。加入心活性类固醇stophanthidin(10 -5 M)后细胞内Na活性的初始升高速率被用于估计净的Na被动流入。5。普鲁卡因(5×10 -4 M)使细胞内Na活性的上升速率降低了50%。所使用的最高普鲁卡因浓度(10 -2 M)使上升速度降低了约80%。6。普鲁卡因(5×10 -3 M)还降低了去除外部K(Ko)所产生的细胞内Na的上升速率,并防止了缺少Ko.7引起的大量去极化。 TTX还降低了添加鸟嘌呤后细胞内Na活性的上升速率。在我们的实验中,当TTX浓度为10 -6 g / ml时,效果最大。在此浓度下,膜电位为-70 mV时,细胞内Na活性的上升速率降低了约40%。8。我们从实验中得出结论,局部麻醉药和TTX对细胞内Na活性的影响是通过降低细胞膜的Na通透性来实现的,并且在正常的静息电位下,Na通过TTX敏感通道进入的作用很大。到总的Na净流入量。

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