Ko S H, Lee S K, Han Y J, Choe H, Kwak Y G, Chae S W, Cho K P, Song H S
Chonbuk National University Medical School, Keum-Am Dong Chonju, Korea.
Anesthesiology. 1997 Jul;87(1):68-74. doi: 10.1097/00000542-199707000-00010.
The adenosine triphosphate (ATP)-sensitive potassium (KATP) channel underlies the increase in potassium permeability during hypoxia and ischemia. The increased outward potassium current during ischemia may be an endogenous cardioprotective mechanism. This study was designed to determine the effects of ketamine on KATP channel in rat hearts.
Inside-out and cell-attached configurations of patch-clamp techniques and 3 M potassium chloride-filled conventional microelectrodes were used to investigate the effect of ketamine on KATP channel currents in single rat ventricular myocytes and on the action potential duration of rat papillary muscles, respectively.
Ketamine inhibited KATP channel activity in rat ventricular myocytes in a concentration-dependent manner. In the inside-out patches, the concentration of ketamine for half-maximal inhibition and the Hill coefficient were 62.9 microM and 0.54, respectively. In a concentration-dependent manner, ketamine inhibited pinacidil- and 2,4-dinitrophenol-activated KATP channels in cell-attached patches. The application of ketamine to the intracellular side of membrane patches did not affect the conduction of single-channel currents of KATP channels. Ketamine increased the action potential duration, which was then shortened by pinacidil in a concentration-dependent manner.
Ketamine inhibited KATP channel activity in a concentration-dependent manner. These results suggest that ketamine may attenuate the cardioprotective effects of the KATP channel during ischemia and reperfusion in the rat myocardium.
三磷酸腺苷（ATP）敏感性钾（KATP）通道是缺氧和缺血期间钾通透性增加的基础。缺血期间外向钾电流增加可能是一种内源性心脏保护机制。本研究旨在确定氯胺酮对大鼠心脏KATP通道的影响。
采用膜片钳技术的内面向外和细胞贴附模式以及3M氯化钾填充的传统微电极，分别研究氯胺酮对单个大鼠心室肌细胞KATP通道电流和大鼠乳头肌动作电位时程的影响。
氯胺酮以浓度依赖性方式抑制大鼠心室肌细胞的KATP通道活性。在内面向外的膜片中，氯胺酮半数最大抑制浓度和希尔系数分别为62.9微摩尔和0.54。氯胺酮以浓度依赖性方式抑制细胞贴附膜片中吡那地尔和2,4-二硝基苯酚激活的KATP通道。将氯胺酮应用于膜片的细胞内侧不影响KATP通道单通道电流的传导。氯胺酮增加动作电位时程，然后吡那地尔以浓度依赖性方式使其缩短。
氯胺酮以浓度依赖性方式抑制KATP通道活性。这些结果表明，氯胺酮可能会减弱大鼠心肌缺血再灌注期间KATP通道的心脏保护作用。
