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低钾血症腺苷-利多卡因心脏停搏液:维持极化心肌以实现最佳停搏和复律的重要性。

Normokalemic adenosine-lidocaine cardioplegia: importance of maintaining a polarized myocardium for optimal arrest and reanimation.

机构信息

Heart Research Laboratory, Department of Physiology and Pharmacology, Molecular Science Building, James Cook University, Townsville, Queensland 4811, Australia.

出版信息

J Thorac Cardiovasc Surg. 2010 Jun;139(6):1576-86. doi: 10.1016/j.jtcvs.2009.10.013. Epub 2010 Feb 4.

Abstract

OBJECTIVE

Depolarizing potassium cardioplegia does not afford optimal cardioprotection in pediatric or adult patients requiring complicated operative procedures. Polarizing adenosine-lidocaine cardioplegia has been shown to be cardioprotective without hyperkalemia. Our aim was to examine the effects of changing extracellular potassium levels in adenosine-lidocaine cardioplegia on arrest and reanimation properties.

METHODS

Isolated-perfused rat hearts (n = 96) were arrested at 32 degrees C to 33 degrees C for 1 or 2 hours with intermittent 200 mumol/L adenosine and 500 mumol/L lidocaine in modified Krebs-Henseleit buffer with 0.1, 3.0, 5.9, 10, and 16 mmol/L potassium or with 16 or 25 mmol/L potassium in Krebs-Henseleit buffer (n = 8 for each group). Membrane potentials were estimated in the arrested ventricular myocardium (n = 42), and recovery function was measured in working mode during 60 minutes' reperfusion.

RESULTS

Arrest was interrupted by breakout beats in the adenosine-lidocaine hypokalemic (0.1 and 3 mmol/L potassium) and non-adenosine-lidocaine hyperkalemic (16 and 25 mmol/L potassium) groups. The membrane potentials for the non-adenosine-lidocaine 16 and 25 mmol/L potassium groups were -51 and -39 mV, and those for the adenosine-lidocaine groups (0.1, 3.0, 5.9, 10, and 16 mmol/L potassium) were -183, -94, -75, -65, and -49 mV, respectively. After 1 hour of arrest, coronary vascular resistance increased linearly in adenosine-lidocaine cardioplegia with increasing potassium levels (5.9, 10, and 16 mmol/L), and the slope increased more than 2-fold after 2 hours. Nearly 40% of hearts in the adenosine-lidocaine (0.1 mmol/L potassium) and non-adenosine-lidocaine 25 mmol/L potassium groups failed to recover after 1 hour arrest. After 2 hours, hearts in the polarizing (5.9 mmol/L potassium) adenosine-lidocaine group increased coronary vascular resistance by only 30% and spontaneously recovered 107% heart rate, 92% systolic pressure, 81% aortic flow, and 113% coronary flow (all metrics returned 85% to 100% at 15 minutes) with no reperfusion arrhythmias. In contrast, hearts in the adenosine-lidocaine (3, 10, and 16 mmol/L potassium) groups were all slow to recover (15% to 40% return at 15 minutes) and experienced arrhythmias. Increasing potassium levels in adenosine-lidocaine cardioplegia from 5.9 to 16 mmol/L resulted in a 67% loss of left ventricular contractility.

CONCLUSIONS

Polarizing adenosine-lidocaine cardioplegia (5.9 mmol/L potassium) administered intermittently at 33 degrees C provides superior arrest and reanimation profiles under normokalemic conditions when the myocardial cell membrane potential is close to its resting state.

摘要

目的

在需要复杂手术的儿科或成年患者中,去极化钾心脏停搏液不能提供最佳的心脏保护作用。极化的腺苷-利多卡因心脏停搏液已被证明具有心脏保护作用,而不会引起高钾血症。我们的目的是研究改变腺苷-利多卡因心脏停搏液中细胞外钾水平对停搏和复律特性的影响。

方法

在 32°C 至 33°C 下用间歇性 200 μmol/L 腺苷和 500 μmol/L 利多卡因在改良 Krebs-Henseleit 缓冲液中对离体灌注大鼠心脏(n = 96)进行 1 或 2 小时的心脏停搏,缓冲液中的钾浓度分别为 0.1、3.0、5.9、10 和 16 mmol/L 或 16 或 25 mmol/L (每组 n = 8)。在停搏的心室心肌中估计膜电位(n = 42),并在 60 分钟再灌注期间测量工作模式下的恢复功能。

结果

在腺苷-利多卡因低钾(0.1 和 3 mmol/L 钾)和非腺苷-利多卡因高钾(16 和 25 mmol/L 钾)组中,心脏停搏被突破搏动打断。非腺苷-利多卡因 16 和 25 mmol/L 钾组的膜电位为-51 和-39 mV,而腺苷-利多卡因组(0.1、3.0、5.9、10 和 16 mmol/L 钾)的膜电位分别为-183、-94、-75、-65 和-49 mV。停搏 1 小时后,随着钾水平的升高(5.9、10 和 16 mmol/L),腺苷-利多卡因心脏停搏液中的冠状动脉血管阻力呈线性增加,2 小时后斜率增加了 2 倍以上。在腺苷-利多卡因(0.1 mmol/L 钾)和非腺苷-利多卡因 25 mmol/L 钾组中,约 40%的心脏在停搏 1 小时后无法恢复。停搏 2 小时后,极化(5.9 mmol/L 钾)腺苷-利多卡因组的冠状动脉血管阻力仅增加 30%,并自发恢复 107%心率、92%收缩压、81%主动脉流量和 113%冠脉流量(所有指标在 15 分钟时恢复 85%至 100%),无再灌注心律失常。相比之下,腺苷-利多卡因(3、10 和 16 mmol/L 钾)组的心脏恢复缓慢(15 分钟时恢复 15%至 40%),并出现心律失常。将腺苷-利多卡因心脏停搏液中的钾水平从 5.9 增加到 16 mmol/L 会导致左心室收缩力丧失 67%。

结论

在正常血钾条件下,当心肌细胞膜电位接近静息状态时,间歇性 33°C 给予极化的腺苷-利多卡因心脏停搏液(5.9 mmol/L 钾)可提供更好的停搏和复律特性。

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