羧甲基壳聚糖对大鼠单一心房肌细胞超速激活延迟整流钾电流的作用

Effect of carboxymethyl chitosan on ultrarapid delayed rectifier potassium current in single atrial myocyte of rats

目的 探讨羧甲基壳聚糖 (CMCS)对心血管作用的机制。方法 利用膜片钳全细胞记录方式 ,双脉冲方波刺激 ,首先给一个时程为 2 0 0ms ,保持电位 - 6 0mV ,去极化到 +30mV的条件脉冲 ,间隔 2 0ms后 ,再给予波宽 12 0 0ms的方波刺激 ,保持电位- 6 0mV ,刺激电压从 - 40mV～ +5 0mV ,步阶电压10mV。结果 CMCS抑制IKur,当其浓度为 1和 2g·L- 1时 ,指令电位 +5 0mV的电流值分别由给药前的 ( 1.8± 0 .7)和 ( 2 .0± 0 .6 )nA下降到 ( 1.6± 0 .6 )(n =12 ,P <0 .0 1)和 ( 1.5± 0 .5 )nA (n =7,P <0 .0 1)。其他指令电位下的IKur的改变也符合此趋势。增加刺激频率及指令电压IKur的变化均不显著 ,提示CMCS对IKur的抑制作用不具有电压依赖性和频率依赖性。结论 CMCS可抑制大鼠单一心房肌细胞IKur。

AIM To study the mechanism of cardiovascular effect of carboxymethyl chitosan (CMCS). METHODS Whole cell patch clamp technique was used. The stimulating protocol was holding potential -60 mV, stimulating potential -40 mV to +50 mV, step potential +10 mV, duration 1200 ms, stimulating interval 3 s and stimulating frequency 2 Hz, preceded by a 200 ms prepulse to +30 mV; the distance between the prepulse and test pulse was 20 ms. RESULTSWhen holding potential was -60 mV and stimulating potential was +50 mV, IKur reduced from (1.8±0.7) and (2.0±0.6)nA to (1.6±0.6) (n=12, P<0.01) and (1.5±0.5)nA (n=7, P<0.01), respectively, after 1 and 2 g·L-1 CMCS were added to extracellular solution. The changes in IKur were consistent with this under other commanding potentials. With the increases in stimulating frequency and commanding potential, no significant change in IKur was seen. The results suggested CMCS inhibit IKur in a voltage independent and frequency independent manners. CONCLUSION CMCS inhibits IKur in single atrial myocyte of rats.