Effects of anesthetic-induced preconditioning on mitochondrial ion channels

我们研究了线粒体离子通道的电生理特征，这被认为是麻醉诱导预处理的重要因素。钙超载是引发心脏缺血再灌注损伤的重要机制。Ryanodine受体作为钙诱导的钙释放介质在肌细胞中起重要作用。我们发现了几种类型的线粒体离子通道，其中一种可能是线粒体ryanodine受体。同时记录心脏钠电流。APC导致钠电流密度增大。这种变化与钠离子通道表达的增加有关。稳态失活曲线明显向去极化方向偏移，失活恢复明显加快。APC引起的这些电生理变化不影响动作电位模拟。

We studied electrophysiological profiles of mitochondrial ion channels, which are known as important factors in anesthetic-induced preconditioning. Calcium overload is crucial mechanism to trigger cardiac ischemia/reperfusion injury. Ryanodine receptors play an important role as a mediator of calcium-induced calcium release in myocytes. We found several types of mitochondrial ion channels, and one of them may be mitochondrial ryanodine receptors. Cardiac sodium current was also recorded. APC resulted in the increase of the sodium current density. This change was correlated with the increase of the sodium channel expression. The steady-state inactivation curve was significantly shifted toward depolarizing direction, and recovery from inactivation was significantly accelerated. These electrophysiological changes by APC did not affect the action potential simulation.