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研究羧甲基壳聚糖对豚鼠单一心室肌细胞延迟外向钾电流 (IK)的作用 ,从离子通道角度初步探讨其作用机理。应用膜片钳全细胞记录方式 ,设保持电位为 - 50 m V,指令电位为 - 50~ +70 m V,步阶脉冲 1 0 m V,刺激频率 1 Hz,波宽 1 0 0 0 ms,刺激间隔 5s的方波钳制方案。羧甲基壳聚糖能抑制 IK,并呈浓度依赖关系。选择指令电位 +70 m V时给药前后 IK 的变化进行统计 ,当浓度为 0 .1 %时 ,IK由给药前的 1 .1 6± 0 .30 n A减少至药后的 0 .96± 0 .2 7n A(n=4,P<0 .0 1 ) ,其抑制率是 1 7.70± 0 .0 5%。当浓度为 0 .2 %时 ,IK 由给药前的 1 .46±0 .62 n A减少至给药后的 1 .0 6± 0 .49n A(n=4,P<0 .0 1 ) ,抑制率是 2 8.66± 0 .0 6%。其它指令电位下的 IK 的改变也符合此趋势。羧甲基壳聚糖抑制豚鼠单一心室肌细胞延迟外向 K+ 电流。
To study the effect of carboxymethyl chitosan on the delayed outward potassium current (IK) in guinea pig single ventricular myocytes, and to explore its mechanism from the ion channel perspective. Patch-clamp whole-cell recording was used. The holding potential was -50 mV, the command potential was -50 ~ +70 mV, the step pulse was 10 mV, the stimulation frequency was 1 Hz, the wave length was 100 000 ms, Stimulation interval 5s square wave clamping scheme. Carboxymethyl chitosan inhibited IK in a concentration-dependent manner. When the command potential was +70 mV, the changes of IK before and after administration were counted. When the concentration was 0.1%, IK decreased from 1.16 ± 0.30 n A before administration to 0.96 after administration ± 0.27nA (n = 4, P <0.01), the inhibition rate was 1.70 ± 0.55%. When the concentration was 0.2%, the IK decreased from 1.46 ± 0.62 n A before administration to 1.06 ± 0.49 n A after administration (n = 4, P <0.01) ), The inhibition rate is 2 8.66 ± 0. 06%. Changes in IK under other command potentials also comply with this trend. Carboxymethyl chitosan inhibits delayed outward K + currents in guinea pig single ventricular myocytes.