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动作电位时程交替和乌头碱诱发心律失常在离体兔心中的作用。

Role of the alternans of action potential duration and aconitine-induced arrhythmias in isolated rabbit hearts.

机构信息

Department of Cardiology, Fatima General Hospital, Daegu, Korea.

出版信息

J Korean Med Sci. 2011 Dec;26(12):1576-81. doi: 10.3346/jkms.2011.26.12.1576. Epub 2011 Nov 29.

DOI:10.3346/jkms.2011.26.12.1576
PMID:22147994
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3230017/
Abstract

Under conditions of Na(+) channel hyperactivation with aconitine, the changes in action potential duration (APD) and the restitution characteristics have not been well defined in the context of aconitine-induced arrhythmogenesis. Optical mapping of voltage using RH237 was performed with eight extracted rabbit hearts that were perfused using the Langendorff system. The characteristics of APD restitution were assessed using the steady-state pacing protocol at baseline and 0.1 µM aconitine concentration. In addition, pseudo-ECG was analyzed at baseline, and with 0.1 and 1.0 µM of aconitine infusion respectively. Triggered activity was not shown in dose of 0.1 µM aconitine but overtly presented in 1.0 µM of aconitine. The slopes of the dynamic APD restitution curves were significantly steeper with 0.1 µM of aconitine than at baseline. With aconitine administration, the cycle length of initiation of APD alternans was significantly longer than at baseline (287.5 ± 9.6 vs 247.5 ± 15.0 msec, P = 0.016). The functional reentry following regional conduction block appears with the progression of APD alternans. Ventricular fibrillation is induced reproducibly at pacing cycle length showing a 2:1 conduction block. Low-dose aconitine produces arrhythmogenesis at an increasing restitution slope with APD alternans as well as regional conduction block that proceeds to functional reentry.

摘要

在乌头碱导致的钠通道过度激活的情况下,动作电位时程(APD)的变化和恢复特性在乌头碱致心律失常发生的情况下尚未得到很好的定义。使用 RH237 通过 Langendorff 系统灌注的 8 个提取的兔心进行电压光学映射。在基线和 0.1 µM 乌头碱浓度下使用稳态起搏方案评估 APD 恢复特性。此外,在基线、分别用 0.1 和 1.0 µM 乌头碱输注时分析伪 ECG。在 0.1 µM 乌头碱的剂量下未显示触发活动,但在 1.0 µM 乌头碱中明显呈现。与基线相比,在 0.1 µM 乌头碱时动态 APD 恢复曲线的斜率明显更陡。在用乌头碱给药后,APD 交替的起始周期长度明显长于基线(287.5 ± 9.6 与 247.5 ± 15.0 msec,P = 0.016)。随着 APD 交替的进展,区域性传导阻滞后的功能性折返出现。在显示 2:1 传导阻滞的起搏周期长度下,可重复诱发心室颤动。低剂量乌头碱在 APD 交替和区域性传导阻滞的恢复斜率增加的情况下产生心律失常,这会导致功能性折返。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/505f/3230017/31e7b48567ba/jkms-26-1576-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/505f/3230017/618ae04c1cae/jkms-26-1576-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/505f/3230017/890d38bda7e0/jkms-26-1576-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/505f/3230017/6fb4392810af/jkms-26-1576-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/505f/3230017/31e7b48567ba/jkms-26-1576-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/505f/3230017/618ae04c1cae/jkms-26-1576-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/505f/3230017/890d38bda7e0/jkms-26-1576-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/505f/3230017/6fb4392810af/jkms-26-1576-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/505f/3230017/31e7b48567ba/jkms-26-1576-g004.jpg

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