Role of apamin-sensitive small conductance calcium-activated potassium currents in long-term cardiac memory in rabbits.
Role of apamin-sensitive small conductance calcium-activated potassium currents in long-term cardiac memory in rabbits.
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DOI：
10.1016/j.hrthm.2018.01.016
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发表时间：
2018-05
期刊：
影响因子：
5.5
通讯作者：
Everett TH 4th
中科院分区：
文献类型：
--
作者：
Yin D;Chen M;Yang N;Wu AZ;Xu D;Tsai WC;Yuan Y;Tian Z;Chan YH;Shen C;Chen Z;Lin SF;Weiss JN;Chen PS;Everett TH 4th
阿帕明敏感的小电导钙激活钾电流(IKAS)在心室起搏过程中上调，并掩盖短期心脏记忆(CM)。以确定IKAS在长期CM中的作用。CM是通过3-5周的心室起搏创建的，以停止起搏时的平坦或倒置T波为定义。心外膜光学标测是在起搏和正常脑室中进行的。起搏时测定动作电位时程(APD80)。测定IKAS阻断前后的室壁稳定性。取4例起搏心脏和4例正常心脏进行免疫印迹和组织学观察。两组之间的超声心动图参数或纤维化水平均无显著差异。阿帕明可使心肌的APD80延长(9.6%[8.8%-10.5%]vs3.1%[1.9%-4.3%]，p<；0.001)。Apamin显著延长了CM模型中晚期激活位点的APD80，表明这些位点的IKA显著上调。CM模型还改变了对钙的处理，因为50%的钙瞬变持续时间和幅度在远端部位比近端部位(靠近起搏部位)增加。应用阿帕明后，CM模型的室颤诱发率增加(33/40(82.5%)vs 7/20(35%)P&0.001)，室颤持续时间延长(124vs 26s，P<；0.001)。慢性心室起搏增加晚期激活部位的钙瞬变，从而激活IKAS以维持复极储备。IKAS受体阻滞剂增加了慢性起搏的兔心室室颤易损性。
Apamin-sensitive small conductance calcium-activated K current (IKAS) is upregulated during ventricular pacing and masks short-term cardiac memory (CM). To determine the role of IKAS in long-term CM. CM was created with 3-5 weeks of ventricular pacing and defined by a flat or inverted T-wave off pacing. Epicardial optical mapping was performed in both paced and normal ventricles. Action potential duration (APD80) was determined during RA pacing. Ventricular stability was tested before and after IKAS blockade. Four paced hearts and 4 normal hearts were used for western blotting and histology. There were no significant differences in either the echocardiographic parameters or in fibrosis levels between groups. Apamin induced more APD80 prolongation in CM than in normal ventricles (9.6% [8.8%-10.5%] vs 3.1% [1.9%-4.3%], p<0.001). Apamin significantly lengthend the APD80 in the CM model at late activation sites, indicating significant IKAS upregulation at those sites. The CM model also had altered Ca2+ handling as the 50% Ca2+ transient duration and amplitude were increased at distal sites compared to a proximal site (near the pacing site). After apamin, the CM model had increased VF inducibility (paced vs control, 33/40 (82.5%) vs 7/20 (35%) P<0.001), and longer VF durations (124 vs 26 seconds, P<0.001). Chronic ventricular pacing increases Ca2+ transients at late activation sites which activates IKAS to maintain repolarization reserve. IKAS blockade increases VF vulnerability in chronically paced rabbit ventricles.
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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：
3.7
作者：
Turker I;Yu CC;Chang PC;Chen Z;Sohma Y;Lin SF;Chen PS;Ai T
通讯作者：
Ai T
影响因子：
10.8
作者：
Spragg, DD;Akar, FG;Kass, DA
通讯作者：
Kass, DA
影响因子：
37.8
作者：
Chan YH;Tsai WC;Ko JS;Yin D;Chang PC;Rubart M;Weiss JN;Everett TH 4th;Lin SF;Chen PS
通讯作者：
Chen PS
DOI：
10.1152/ajpheart.00213.2013
发表时间：
2013-08-01
影响因子：
4.8
作者：
Jeyaraj, Darwin;Wan, Xiaoping;Rosenbaum, David S.
通讯作者：
Rosenbaum, David S.