Cha Y M, Uchida T, Wolf P L, Peters B B, Fishbein M C, Karagueuzian H S, Chen P S
Department of Medicine, University of California, San Diego, USA.
Am J Physiol. 1995 Dec;269(6 Pt 2):H1998-2009. doi: 10.1152/ajpheart.1995.269.6.H1998.
The mechanism by which an endocardial-epicardial activation rate gradient develops after 1 or 2 min of sustained ventricular fibrillation is unknown. We recorded from electrodes on the epicardium and from hook electrodes in the endocardium in three open-chest control dogs during prolonged ventricular fibrillation. The same recordings were also made in seven dogs after right ventricular subendocardial ablation with Lugol solution and in three dogs after substitution of air for the cavitary blood. The effects of these interventions, i.e., Lugol ablation (n = 2) and the exposure to air (n = 2), on the subendocardial Purkinje fiber transmembrane action potential properties were also evaluated in vitro using microelectrode recording techniques. The in vivo studies showed a significant endocardial-epicardial rate gradient in the control dogs and in dogs that had air substituted for the cavitary blood. In comparison, in dogs that underwent chemical subendocardial ablation, the activation cycle lengths for the endocardium and epicardium were not significantly different. The in vitro studies showed that subendocardial Purkinje fiber action potentials could still be recorded for up to 10 min of exposure to air. In comparison, in the tissues subjected to chemical ablation, no transmembrane action potentials could be recorded from either the Purkinje fibers or superficial ventricular muscle cells. We conclude that the development of an endocardial-epicardial activation rate gradient during prolonged ventricular fibrillation depends on the presence of intact subendocardial Purkinje fibers and ventricular myocytes. The retained cavitary blood is not responsible for the development of the rate gradient.
持续性室颤1或2分钟后心内膜 - 心外膜激动速率梯度形成的机制尚不清楚。我们在三只开胸对照犬持续性室颤期间，记录了心外膜电极和心内膜钩状电极的数据。在七只经卢戈氏溶液进行右心室心内膜下消融的犬以及三只将心腔内血液置换为空气的犬中也进行了同样的记录。还使用微电极记录技术在体外评估了这些干预措施，即卢戈氏消融（n = 2）和暴露于空气（n = 2）对心内膜下浦肯野纤维跨膜动作电位特性的影响。体内研究显示，对照犬以及心腔内血液被空气置换的犬存在显著的心内膜 - 心外膜速率梯度。相比之下，在进行化学性心内膜下消融的犬中，心内膜和心外膜的激动周期长度无显著差异。体外研究表明，暴露于空气长达10分钟仍可记录到心内膜下浦肯野纤维动作电位。相比之下，在接受化学消融的组织中，无论是浦肯野纤维还是心室表层肌细胞均未记录到跨膜动作电位。我们得出结论，持续性室颤期间心内膜 - 心外膜激动速率梯度的形成取决于完整的心内膜下浦肯野纤维和心室肌细胞的存在。保留的心腔内血液并非速率梯度形成的原因。
