麻醉药物对窦房结自律性的离子作用机制
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Ionic mechanisms of the action of anaesthetics on sinoatrial node automaticity
摘要翻译
临床上各种全身麻醉药会影响心率，但其明确的机制尚不清楚。由于心率由心脏起搏位置窦房结的自律性及自主神经系统的调节而决定，所以研究麻醉药对窦房结自律性的影响是十分必要的。
窦房结的自发性电活动是一个多离子电流相互协调的过程，如：超极化激活阳离子电流（IF）、T型 和L型钙电流（ICa2+，T和ICa2+，L）、Na+/Ca2+交换电流（INCX）、延迟整流钾电流的快激活成分及慢激活成分（Ikr和IKs）。
膜片钳技术研究表明不同麻醉药对窦房结自律性及其潜在离子电流具有直接抑制作用。七氟醚，地氟醚和丙泊酚通过抑制多种离子通道及其转运功能，如：If、ICa2+，T、ICa2+，L、IKs和INCX，从而直接抑制窦房结的自律性。
麻醉药物对多种离子通道和转运功能的抑制作用可纳入窦房结模型，在计算机模拟中麻醉药物抑制窦房结活动的现象可有效复制。麻醉药物对窦房结节自律性的抑制作用在某些病理生理条件更明显，如：衰老、心力衰竭和心律不齐，此时参与窦房结节自律性的离子通道功能发生变化。
本综述主要从分子、离子通道和细胞机制等层面，总结麻醉药物对窦房结自律性的调节作用，为围术期心率变化提供电生理和分子基础。
原始文献摘要
Akiko Kojimaa, Hiroshi Matsuurab. Ionic mechanisms of the action of anaesthetics on sinoatrial node automaticity .European Journal of Pharmacology 2017.5
Abstract ：
Although various general anaesthetics affect the heart rate in clinical settings, their precise mechanisms remain to be fully elucidated. Because the heart rate is determined by automaticity of the cardiac pacemaker sinoatrial node and its regulation by autonomic nervous system, it is important to clarify the effect of anaesthetics on sinoatrial node automaticity.
The spontaneous electrical activity of sinoatrial node is generated by a complex but coordinated interaction of multiple ionic currents, such as the hyperpolarisation-activated cation current (If), Ttype and L-type Ca2+ currents (ICa,T and ICa,L), Na+/Ca2+ exchange current (INCX), and rapidly and slowly activating delayed rectifier K+ currents (IKr and IKs).
Patch-clamp studies have revealed the direct inhibitory effects of various anaesthetics on sinoatrial node automaticity and its underlying ionic mechanisms. Sevoflurane, desflurane and propofol directly suppress the sinoatrial node automaticity by inhibiting multiple ionic channels and transporter, such as If, ICa,T, ICa,L, IKs and INCX.
By incorporating these inhibitory effects of anaesthetics on multiple ion channels and transporter into sinoatrial node model, suppression of sinoatrial node activity is well reproduced in computer simulation. The inhibitory effect of anaesthetics on sinoatrial node automaticity can be exaggerated under some pathophysiological conditions, such as aging, heart failure and arrhythmias, where the function and/or expression of ion channels involved in sinoatrial node automaticity are modulated.
This review focuses on molecular, ionic and cellular mechanisms underlying the regulation of sinoatrial node automaticity by anaesthetics, which will provide an electrophysiological and molecular basis for understanding the changes in heart rate during perioperative period.
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