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本研究应用全细胞膜片钳技术观察氯胺酮对人心房肌细胞瞬时外向钾电流(transient outward potassium current,Ito)的影响,以了解其作用的部分机制。标本取自心脏瓣膜置换病人的右心耳,采用急性酶解法消化分离人心房肌细胞,室温下以全细胞膜片钳技术记录Ito,分别观察30、100、300和1000μmol·L-1的氯胺酮对Ito的作用。实验过程由pCLAMP9.0软件程序发放刺激和采集信号并存储于计算机中。结果表明,氯胺酮对Ito电流-电压曲线呈浓度依赖性抑制作用,在+50mV时,30、100、300和1000μmol·L-1的氯胺酮分别阻断Ito峰电流(13.62±0.04)%、(38.92±0.05)%、(72.24±0.10)%和(83.84±0.05)%,其半数有效浓度(IC50)为121μmol·L-1。但是100μmol·L-1氯胺酮对Ito的激活和失活曲线以及复活曲线均无明显影响。由此得知,氯胺酮呈浓度依赖性抑制人心房肌细胞瞬时外向钾电流。
In this study, whole-cell patch clamp technique was used to observe the effect of ketamine on transient outward potassium current (Ito) in human atrial myocytes, in order to understand its mechanism. The specimens were obtained from the heart atrial appendage of patients with right atrial appendage. The human atrial myocytes were digested by acute enzymatic digestion, and Ito was recorded by whole-cell patch clamp technique at room temperature. The effects of 30, 100, 300 and 1000 μmol·L-1 ketamine on Ito Role. Experimental process by the pCLAMP9.0 software program issued stimulation and acquisition signals and stored in the computer. The results showed that Ketamine inhibited the Ito current-voltage curve in a concentration-dependent manner. At +50 mV, 30,100,300 and 1000μmol·L-1 Ketamine blocked Ito peak current (13.62 ± 0.04)%, (38.92% ± 0.05%, (72.24 ± 0.10)% and (83.84 ± 0.05)% respectively. The IC50 was 121μmol·L-1. However, 100μmol·L-1 ketamine had no significant effect on Ito activation and inactivation and resuscitation curves. It was found that ketamine in a concentration-dependent inhibition of human atrial myocytes transient outward potassium current.