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首页> 外文期刊>American Journal of Physiology >Ketamine abolishes ischemic preconditioning through inhibition of K(ATP) channels in rabbit hearts.
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Ketamine abolishes ischemic preconditioning through inhibition of K(ATP) channels in rabbit hearts.

机译：氯胺酮通过抑制兔心脏中的K（ATP）通道消除了缺血性预处理。

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摘要

Although ketamine inhibits ATP-sensitive K (K(ATP)) channels in rat ventricular myocytes and abolishes the cardioprotective effect of ischemic preconditioning in isolated rat hearts and in rabbits in in vivo, no studies to date specifically address the precise mechanism of this prevention of ischemic preconditioning by ketamine. This study investigated the mechanism of the blockade of ischemic preconditioning by ketamine in rabbit ventricular myocytes using patch-clamp techniques and in rabbit heart slices model for simulated ischemia and preconditioning. In cell-attached and inside-out patches, ketamine inhibited sarcolemmal K(ATP) channel activities in a concentration-dependent manner. Ketamine decreased the burst duration and increased the interburst duration without a change in the single-channel conductance. In the heart slice model of preconditioning, heart slices preconditioned with a single 5-min anoxia, pinacidil, or diazoxide, followed by 15-min reoxygenation, were protected against subsequent 30-min anoxia and 1-h reoxygenation, and the cardioprotection was blocked by the concomitant presence of ketamine. These data are consistent with the notion that inhibition of sarcolemmal or mitochondrial K(ATP) channels may contribute, at least in part, to the mechanism of the blockade of ischemic preconditioning by ketamine.
机译：尽管氯胺酮抑制大鼠心室肌细胞中的ATP敏感性K（K（ATP））通道，并在体内离体的大鼠心脏和家兔中取消了缺血预处理的心脏保护作用，但迄今为止尚无任何研究专门针对这种预防心律失常的确切机制进行研究。氯胺酮可进行缺血预处理。本研究使用膜片钳技术研究了氯胺酮对兔心室肌细胞局部缺血预处理的机制，并在模拟心脏缺血和预处理的兔心脏切片模型中进行了研究。在细胞附着和由内而外的补丁中，氯胺酮以浓度依赖的方式抑制肌膜钾离子通道的活性。氯胺酮在不改变单通道电导的情况下减少了爆发持续时间并增加了爆发持续时间。在预处理的心脏切片模型中，对经过单次5分钟缺氧，吡那地尔或二氮嗪进行预处理的心脏切片，然后进行15分钟的复氧，可防止随后的30分钟缺氧和1小时的复氧，并且心脏保护功能被阻断氯胺酮的同时存在。这些数据与抑制肌膜或线粒体K（ATP）通道可能至少部分有助于氯胺酮阻断缺血预处理的机制相一致。

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