Does the combination of hyperkalemia and KATP activation determine excitation rate gradient and electrical failure in the globally ischemic fibrillating heart?
Does the combination of hyperkalemia and KATP activation determine excitation rate gradient and electrical failure in the globally ischemic fibrillating heart?
复制标题
高钾血症和 KATP 激活的结合是否决定了整体缺血性颤动心脏的兴奋率梯度和电衰竭？
DOI：
10.1152/ajpheart.00184.2013
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发表时间：
2013
期刊：
影响因子：
--
通讯作者：
Zaitsev,AlexeyV
中科院分区：
文献类型：
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作者：
Taylor,TysonG;Venable,PaulW;Booth,Alicja;Garg,Vivek;Shibayama,Junko;Zaitsev,AlexeyV
全球缺血性心脏中的心室颤动（VF）的特点是进行性电抑制，表现为 VF 兴奋率（VFR）下降和兴奋性丧失，首先发生在心外膜下（Epi）并扩散到心内膜下（Endo）。早期电气故障不利于心脏骤停期间成功的除颤和复苏。高钾血症和/或 ATP 敏感 K+ (KATP) 通道的激活与电衰竭有关，但这些因素在缺血性心室颤动中的作用尚不清楚。我们确定了全球缺血心脏（Isch 组）和高钾血症（HighK 组）或高钾血症和 KATP 通道开放剂 Cromakalim 组合（HighK-Crom 组）的含氧量正常心脏的 VF 期间左心室 Endo 和 Epi 的 VFR 与细胞外 K+浓度 ([K+]o) 的关系。在Isch组中，比较缺血性VF早期（0-6分钟）、中期（7-13分钟）和晚期（14-20分钟）阶段的[K+]o和VFR的Endo和Epi值。在所有三个阶段均观察到 VFR 的显着透壁梯度（Endo > Epi），而 [K+]o（Epi > Endo）的显着透壁梯度仅发生在缺血性 VF 的晚期。在 Isch 组中，VFR 降低和兴奋性开始在比 HighK 组低得多的 [K+]o 时发生，特别是在 Epi 中。将 KATP 激活与高钾血症相结合只会使 VFR-[K+] 曲线向上移动（与真正缺血相反的效果），而不会改变心搏停止的 [K+] 阈值。我们的结论是，高钾血症和/或 KATP 激活不能充分解释缺血性 VF 期间的异质性电抑制和电衰竭。
Ventricular fibrillation (VF) in the globally ischemic heart is characterized by a progressive electrical depression manifested as a decline in the VF excitation rate (VFR) and loss of excitability, which occur first in the subepicardium (Epi) and spread to the subendocardium (Endo). Early electrical failure is detrimental to successful defibrillation and resuscitation during cardiac arrest. Hyperkalemia and/or the activation of ATP-sensitive K+(KATP) channels have been implicated in electrical failure, but the role of these factors in ischemic VF is poorly understood. We determined the VFR-extracellular K+concentration ([K+]o) relationship in the Endo and Epi of the left ventricle during VF in globally ischemic hearts (Isch group) and normoxic hearts subjected to hyperkalemia (HighK group) or a combination of hyperkalemia and the KATPchannel opener cromakalim (HighK-Crom group). In the Isch group, Endo and Epi values of [K+]oand VFR were compared in the early (0–6 min), middle (7–13 min), and late (14–20 min) phases of ischemic VF. A significant transmural gradient in VFR (Endo > Epi) was observed in all three phases, whereas a significant transmural gradient in [K+]o(Epi > Endo) occurred only in the late phase of ischemic VF. In the Isch group, the VFR decrease and inexcitability started to occur at much lower [K+]othan in the HighK group, especially in the Epi. Combining KATPactivation with hyperkalemia only shifted the VFR-[K+]ocurve upward (an effect opposite to real ischemia) without changing the [K+]othreshold for asystole. We conclude that hyperkalemia and/or KATPactivation cannot adequately explain the heterogeneous electrical depression and electrical failure during ischemic VF.