Sabir Ian N, Fraser James A, Killeen Matthew J, Grace Andrew A, Huang Christopher L-H
Physiological Laboratory, University of Cambridge, Downing Street, Cambridge, UK.
Pflugers Arch. 2007 May;454(2):209-22. doi: 10.1007/s00424-007-0217-3. Epub 2007 Feb 13.
The clinical effects of hypokalemia including action potential prolongation and arrhythmogenicity suppressible by lidocaine were reproduced in hypokalemic (3.0 mM K(+)) Langendorff-perfused murine hearts before and after exposure to lidocaine (10 muM). Novel limiting criteria for local and transmural, epicardial, and endocardial re-excitation involving action potential duration (at 90% repolarization, APD(90)), ventricular effective refractory period (VERP), and transmural conduction time (Deltalatency), where appropriate, were applied to normokalemic (5.2 mM K(+)) and hypokalemic hearts. Hypokalemia increased epicardial APD(90) from 46.6 +/- 1.2 to 53.1 +/- 0.7 ms yet decreased epicardial VERP from 41 +/- 4 to 29 +/- 1 ms, left endocardial APD(90) unchanged (58.2 +/- 3.7 to 56.9 +/- 4.0 ms) yet decreased endocardial VERP from 48 +/- 4 to 29 +/- 2 ms, and left Deltalatency unchanged (1.6 +/- 1.4 to 1.1 +/- 1.1 ms; eight normokalemic and five hypokalemic hearts). These findings precisely matched computational predictions based on previous reports of altered ion channel gating and membrane hyperpolarization. Hypokalemia thus shifted all re-excitation criteria in the positive direction. In contrast, hypokalemia spared epicardial APD(90) (54.8 +/- 2.7 to 60.6 +/- 2.7 ms), epicardial VERP (84 +/- 5 to 81 +/- 7 ms), endocardial APD(90) (56.6 +/- 4.2 to 63.7 +/- 6.4 ms), endocardial VERP (80 +/- 2 to 84 +/- 4 ms), and Deltalatency (12.5 +/- 6.2 to 7.6 +/- 3.4 ms; five hearts in each case) in lidocaine-treated hearts. Exposure to lidocaine thus consistently shifted all re-excitation criteria in the negative direction, again precisely agreeing with the arrhythmogenic findings. In contrast, established analyses invoking transmural dispersion of repolarization failed to account for any of these findings. We thus establish novel, more general, criteria predictive of arrhythmogenicity that may be particularly useful where APD(90) might diverge sharply from VERP.
在低钾血症(3.0 mM K⁺)的Langendorff灌注小鼠心脏中,在暴露于利多卡因(10 μM)前后,均重现了低钾血症的临床效应,包括动作电位延长和可被利多卡因抑制的致心律失常性。将涉及动作电位持续时间(复极化90%时,APD₉₀)、心室有效不应期(VERP)和跨壁传导时间(Δlatency,酌情)的新的局部和跨壁、心外膜和心内膜再激动限制标准应用于正常血钾(5.2 mM K⁺)和低钾血症心脏。低钾血症使心外膜APD₉₀从46.6±1.2毫秒增加到53.1±0.7毫秒,但使心外膜VERP从41±4毫秒降低到29±1毫秒,左心内膜APD₉₀未改变(58.2±3.7毫秒到56.9±4.0毫秒),但心内膜VERP从48±4毫秒降低到29±2毫秒,左Δlatency未改变(1.6±1.4毫秒到1.1±1.1毫秒;8个正常血钾和5个低钾血症心脏)。这些发现与基于先前关于离子通道门控改变和膜超极化报道的计算预测精确匹配。因此,低钾血症使所有再激动标准正向偏移。相比之下,低钾血症未改变利多卡因处理心脏的心外膜APD₉₀(54.8±2.7毫秒到60.6±2.7毫秒)、心外膜VERP(84±5毫秒到81±7毫秒)、心内膜APD₉₀(56.6±4.2毫秒到63.7±6.4毫秒)、心内膜VERP(80±2毫秒到84±4毫秒)和Δlatency(12.5±6.2毫秒到7.6±3.4毫秒;每种情况5个心脏)。因此,暴露于利多卡因始终使所有再激动标准负向偏移,再次与致心律失常结果精确一致。相比之下,基于复极跨壁离散度的既定分析无法解释这些发现中的任何一项。因此,我们建立了新的、更通用的、预测致心律失常性的标准,在APD₉₀可能与VERP有显著差异的情况下可能特别有用。