Yamazaki M, Ito Y, Hatakeyama N, Masuda A, Shibuya N, Momose Y
Department of Anesthesiology, Toyama Medical and Pharmaceutical University.
Masui. 1993 Jun;42(6):840-7.
The effects of ketamine on Ca(2+)-activated K+ channel currents were studied in dispersed single smooth muscle cells from rabbit portal vein using inside-out patch clamp technique. In a near physiological K+ and Ca2+ gradient, three populations of outward rectangular single currents were recorded in isolated cell membrane of rabbit portal vein at +60 mV membrane potential. These currents were judged as Ca(2+)-activated K+ channel currents since application of EGTA or Apamin in the internal solution inhibited these currents. Application of 10(-5)M or 10(-4)M ketamine inhibited the number of occurrences of channel opening and decreased open times, but did not reduce the amplitudes. When the 10(-3)M ketamine was applied, the Ca(2+)-activated K+ channel currents were abolished. We suggest that the depression of Ca(2+)-activated K+ channel currents may explain the continuous contraction observed in rabbit portal vein at a clinical concentration of ketamine from a point of electrophysiological K+ current study.
采用内面向外式膜片钳技术,研究了氯胺酮对兔门静脉分散的单个平滑肌细胞中钙激活钾通道电流的影响。在接近生理状态的钾离子和钙离子梯度条件下,在膜电位为+60mV时,兔门静脉分离细胞膜上记录到三种外向矩形单电流。这些电流被判定为钙激活钾通道电流,因为在内部溶液中加入乙二醇双四乙酸(EGTA)或蜂毒明肽可抑制这些电流。应用10^(-5)M或10^(-4)M氯胺酮可抑制通道开放次数并缩短开放时间,但不降低电流幅度。当应用10^(-3)M氯胺酮时,钙激活钾通道电流被消除。从电生理钾电流研究的角度来看,我们认为钙激活钾通道电流的抑制可能解释了在临床浓度的氯胺酮作用下兔门静脉中观察到的持续性收缩。