Hypokalemia promotes late phase 3 early afterdepolarization and recurrent ventricular fibrillation during isoproterenol infusion in Langendorff perfused rabbit ventricles.
Hypokalemia promotes late phase 3 early afterdepolarization and recurrent ventricular fibrillation during isoproterenol infusion in Langendorff perfused rabbit ventricles.
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DOI：
10.1016/j.hrthm.2013.12.032
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发表时间：
2014-04
期刊：
影响因子：
5.5
通讯作者：
Chen, Peng-Sheng
中科院分区：
文献类型：
--
作者：
Maruyama, Mitsunori;Ai, Tomohiko;Chua, Su-Kiat;Park, Hyung-Wook;Lee, Young-Soo;Shen, Mark J.;Chang, Po-Cheng;Lin, Shien-Fong;Chen, Peng-Sheng
关键词：
低钾血症和交感神经激活通常与正常和患病心脏中的电风暴（ES）有关。其机制仍不清楚。检验以下假设：IKATP 激活诱导的晚期 3 期早期后除极 (EAD) 是异丙肾上腺素输注和低钾血症期间 ES 机制的基础。对 32 只 Langendorff 灌注的正常兔心脏中的细胞内钙 (Cai) 和膜电压进行光学绘图。基线时反复发作的电诱发心室颤动不会导致自发性心室颤动 (SVF)。异丙肾上腺素输注期间，在正常细胞外钾 ([K+]o) (4.5 mmol/L) 中研究的 15 颗心脏中，有 1 颗 (7%) 发生 SVF；在 2.0 mmol/L [K+]o 中，8 颗心脏中的 3 颗 (38%) 发生；在 1.5 mmol/L [K+]o 中，10 颗心脏中，有 9 颗 (90%) 发生；在 1.5 mmol/L [K+]o 中，7 颗心脏中，有 7 颗 (100%) 发生 SVF。 1.0 mmol/L [K+]o (P<0.001)。光学测绘显示，异丙肾上腺素和低钾血症会增强除颤后的 Cai 瞬态持续时间 (CaiTD) 和异质性缩短的动作电位持续时间 (APD)，导致晚期 3 期 EAD 和 SVF。尽管没有缺血证据，但 IKATP 阻滞剂（格列本脲，5 μmol/L）可逆转除颤后 APD 缩短并抑制所有研究心脏的复发 SVF。在心室颤动发生之前而不是之后给予硝苯地平可以可靠地预防心室颤动复发。 IKr 阻滞剂 (E-4031) 和小电导钙激活钾通道阻滞剂 (apamin) 未能预防复发性 SVF。 β-肾上腺素能刺激和伴随的低钾血症可能导致 IKATP 的非缺血性激活、异质 APD 缩短和 CaiTD 延长，从而引发晚期 3 期 EAD、触发活动和复发性 SVF。 IKATP 抑制可能有助于控制难治性低钾血症期间的 ES。
Hypokalemia and sympathetic activation are commonly associated with electrical storm (ES) in normal and diseased hearts. The mechanisms remain unclear. To test the hypothesis that late phase 3 early afterdepolarization (EAD) induced by IKATP activation underlies the mechanisms of ES during isoproterenol infusion and hypokalemia. Intracellular calcium (Cai) and membrane voltage were optically mapped in 32 Langendorff-perfused normal rabbit hearts. Repeated episodes of electrically-induced VF at baseline did not result in spontaneous VF (SVF). During isoproterenol infusion, SVF occurred in 1 of 15 hearts (7%) studied in normal extracellular potassium ([K+]o) (4.5 mmol/L), 3 of 8 hearts (38%) in 2.0 mmol/L [K+]o, 9 of 10 hearts (90%) in 1.5 mmol/L [K+]o, and 7 of 7 hearts (100%) in 1.0 mmol/L [K+]o (P<0.001). Optical mapping showed isoproterenol and hypokalemia enhanced Cai transient duration (CaiTD) and heterogeneously shortened action potential duration (APD) after defibrillation, leading to late phase 3 EAD and SVF. IKATP blocker (glibenclamide, 5 μmol/L) reversed the post-defibrillation APD shortening and suppressed recurrent SVF in all hearts studied despite no evidence of ischemia. Nifedipine reliably prevented recurrent VF when given before, but not after, the development of VF. IKr blocker (E-4031) and small conductance calcium activated potassium channel blocker (apamin) failed to prevent recurrent SVF. Beta-adrenergic stimulation and concomitant hypokalemia could cause non-ischemic activation of IKATP, heterogeneous APD shortening and prolongation of CaiTD to provoke late phase 3 EAD, triggered activity and recurrent SVF. IKATP inhibition may be useful in managing ES during resistant hypokalemia.
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影响因子：
20.1
作者：
Chua SK;Chang PC;Maruyama M;Turker I;Shinohara T;Shen MJ;Chen Z;Shen C;Rubart-von der Lohe M;Lopshire JC;Ogawa M;Weiss JN;Lin SF;Ai T;Chen PS
通讯作者：
Chen PS
影响因子：
56.9
作者：
Baukrowitz, T;Schulte, U;Fakler, B
通讯作者：
Fakler, B
影响因子：
6.1
作者：
GUIDERI, G
通讯作者：
GUIDERI, G
DOI：
10.1016/s0735-1097(98)00495-1
发表时间：
1998-12-01
影响因子：
24
作者：
Credner, SC;Klingenheben, T;Hohnloser, SH
通讯作者：
Hohnloser, SH
影响因子：
3.5
作者：
Rosati, B;Rocchetti, R;Wanke, E
通讯作者：
Wanke, E