Smith W T, Fleet W F, Johnson T A, Engle C L, Cascio W E
Department of Medicine, Division of Cardiology, University of North Carolina, Chapel Hill 27599-7075, USA.
Circulation. 1995 Nov 15;92(10):3051-60. doi: 10.1161/01.cir.92.10.3051.
This study was designed to test the hypothesis that the loss of cell-to-cell electrical interaction during ischemia modulates the amplitude of ischemia-induced TQ-segment depression (ie, the injury potential) and the occurrence of ventricular fibrillation (VF) during the so-called Ib phase of ventricular arrhythmias.
Regional ischemia was induced by 60 minutes of mid-left anterior descending coronary artery ligation in open-chest swine (n = 10). Cell-to-cell electrical uncoupling was defined as the onset of the terminal rise in whole-tissue resistivity (Rt). Local activation times and TQ-segment changes (injury potential) were determined from unipolar electrograms. Extracellular K+ ([K+]e) and pH (pHe) were measured with plunge-wire ion-selective electrodes. VF occurred in 6 of 10 pigs during regional no-flow ischemia between 19 and 30 minutes after the arrest of perfusion. The occurrence of VF was positively correlated to the onset of cell-to-cell electrical uncoupling (R2 = .885). Cell-to-cell electrical uncoupling superimposed on changes of [K+]e and pHe contributed to the failure of impulse propagation between 19 and 30 minutes after the arrest of perfusion. During ischemia, maximum TQ-segment depression was -10 mV at 19 minutes, after which TQ-segment depression slowly recovered. The onset of the TQ-segment recovery was correlated to the second rise in Rt (R2 = .886).
In the regionally ischemic in situ porcine heart, loss of cell-to-cell electrical interaction is related to the occurrence of VF and changes in the amplitude of the injury current. Cellular electrical uncoupling contributes to failure of impulse propagation in the setting of altered tissue excitability as a result of elevated [K+]e and low pHe. These data indicate that Ib arrhythmias and ECG changes during ischemia are influenced by the loss of cell-to-cell electrical interaction.
本研究旨在验证以下假设，即在缺血期间细胞间电相互作用的丧失会调节缺血诱导的TQ段压低幅度（即损伤电位）以及在所谓的室性心律失常Ib期心室颤动（VF）的发生。
通过开胸猪（n = 10）左前降支冠状动脉结扎60分钟诱导局部缺血。细胞间电脱耦定义为全组织电阻率（Rt）终末上升的开始。从单极电图确定局部激活时间和TQ段变化（损伤电位）。用插入式线离子选择性电极测量细胞外K+（[K+]e）和pH（pHe）。在灌注停止后19至30分钟的局部无复流缺血期间，10头猪中有6头发生VF。VF的发生与细胞间电脱耦的开始呈正相关（R2 = 0.885）。叠加在[K+]e和pHe变化上的细胞间电脱耦导致灌注停止后19至30分钟之间冲动传导失败。缺血期间，19分钟时TQ段最大压低为-10 mV，此后TQ段压低缓慢恢复。TQ段恢复的开始与Rt的第二次上升相关（R2 = 0.886）。
在局部缺血的原位猪心脏中，细胞间电相互作用的丧失与VF的发生和损伤电流幅度的变化有关。由于[K+]e升高和pHe降低，细胞电脱耦导致在组织兴奋性改变的情况下冲动传导失败。这些数据表明，缺血期间的Ib心律失常和心电图变化受细胞间电相互作用丧失的影响。
