Mechanisms and treatment of polymorphic ventricular tachycardia

1. 在这项研究中，我们探讨了直流电击诱导的多形态室性心动过速（PVT）的机制以及各种药物对体外灌注兔心脏PVT的影响。使用我们定制的光学记录系统，用电压敏感染料（di-4-ANEPPS）染色，记录8-32个心室心外膜部位的荧光动作电位信号。常规记录高信噪比（bbb50 db）的稳定光信号，基线漂移小，为-3.6%/min。在动作电位复极期施加10-40V的直流电击，使动作电位延长，心室复极空间弥散增强，引起兴奋的迂回运动，导致pvt。与单相休克相比，双相休克引起的心室复极弥散度更小，PVT发生率更低，持续时间更短。10μM双酰胺可延长心室动作电位，但对传导速度影响较小，而30 μM双酰胺可显著降低心室传导速度。在10μM双酰胺的存在下，直流冲击诱导PVT的易感性略有降低。相比之下，30μM双酰胺的存在大大增加了PVT的脆弱性，诱导的PVT持续时间比对照组长得多。E-4031 （0.1μM）可导致心室动作电位的反向频率依赖性延长，并显著降低PVT的易感性，持续时间缩短。异丙肾上腺素（0.1μM）刺激β肾上腺素能受体导致动作电位缩短，且区域差异较大。在异丙肾上腺素存在的情况下，PVT的持续时间比对照组更长。综上所述，直流电刺激通过增强心室复极的空间不均匀性引发PVT基础上的兴奋迂回运动，药物诱导的ADP弥散可能促进和加重直流电刺激诱导的再入性心动过速。少

1. In this study, we investigated mechanisms underlying DC shock-induced polymorphic ventricular tachycardia (PVT) and effects of various drugs on PVT in rabbit hearts perfused in vitro.2. Fluorescent action potential signals were recorded from 8-32 epicardial sites of ventricles stained with a voltage-sensitive dye (di-4-ANEPPS) with the use of our custom-built optical recording system. Stable optical signals with a high S/N ratio (>50dB) were routinely recorded with a small base-line drift of -3.6%/min.3. Application of DC shocks (10-40V) during the repolarization phase of action potentials caused a prolongation of action potentials and an enhancement of spatial dispersion of ventricular repolarization, giving rise to an initiation of circuitous movement of excitation leading to PVT.4. Biphasic shocks caused less dispersion of ventricular repolarization and lower incidence and shorter duration of PVT than monophasic shocks.5. 10μM disopyramide prolonged ventricular action potentials … More with minimal effects on conduction velocity, whereas 30 μM disopyramide decreased significantly ventricular conduction velocity. In the presence of 10μM disopyramide, vulnerability to PVT induction by DC shock was slightly reduced. In contrast, in the presence of 30μM disopyramide, vulnerability to PVT was greatly increased and induced PVT showed much longer perpetuation than controls. E-4031 (0.1μM) caused a reverse-frequency dependent prolongation of ventricular action potentials and a marked decrease in vulnerability to PVT with shorter perpetuation.6. Stimulation of β adorenergic receptor by isoproterenol (0.1μM) resulted in a shortening of action potentials with considerable regional differences. In the presence of isoproterenol, PVT showed longer perpetuation than controls.7. In conclusion, DC shocks initiate circuitous movement of excitation underlying PVT through an enhancement of spatial inhomogeneity of ventricular repolarization, and drug-induced in ADP dispersion may facilitate and exaggerate DC shock-induced reentrant tachyarrhythmias. Less