麻醉藥物對竇房結自律性的離子作用機制

摘要翻譯：王貴龍 來源：罌粟花

Ionic mechanisms of the action of anaesthetics on sinoatrial node automaticity

摘要翻譯

臨床上各種全身麻醉藥會影響心率，但其明確的機制尚不清楚。由於心率由心臟起搏位置竇房結的自律性及自主神經系統的調節而決定，所以研究麻醉藥對竇房結自律性的影響是十分必要的。

竇房結的自發性電活動是一個多離子電流相互協調的過程，如：超極化激活陽離子電流（IF）、T型 和L型鈣電流（ICa2+，T和ICa2+，L）、Na+/Ca2+交換電流（INCX）、延遲整流鉀電流的快激活成分及慢激活成分（Ikr和IKs）。

膜片鉗技術研究表明不同麻醉藥對竇房結自律性及其潛在離子電流具有直接抑制作用。七氟醚，地氟醚和丙泊酚通過抑制多種離子通道及其轉運功能，如：If、ICa2+，T、ICa2+，L、IKs和INCX，從而直接抑制竇房結的自律性。

麻醉藥物對多種離子通道和轉運功能的抑制作用可納入竇房結模型，在計算機模擬中麻醉藥物抑制竇房結活動的現象可有效複製。麻醉藥物對竇房結節自律性的抑制作用在某些病理生理條件更明顯，如：衰老、心力衰竭和心律不齊，此時參與竇房結節自律性的離子通道功能發生變化。

本綜述主要從分子、離子通道和細胞機制等層面，總結麻醉藥物對竇房結自律性的調節作用，為圍術期心率變化提供電生理和分子基礎。

原始文獻摘要

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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