Triggered firing in pulmonary veins initiated by in vitro autonomic nerve stimulation
Triggered firing in pulmonary veins initiated by in vitro autonomic nerve stimulation
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DOI：
10.1016/j.hrthm.2005.02.012
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发表时间：
2005-06-01
期刊：
影响因子：
5.5
通讯作者：
Lazzara, R
中科院分区：
文献类型：
--
作者：
Patterson, E;Po, SS;Lazzara, R
背景肺静脉袖内的快速放电经常引发房颤。自主神经系统在促进自发放电中的作用是未知的。结论本研究的目的是确定是否自主神经刺激犬心房和肺静脉袖开始心律失常的形成。方法细胞外双极和细胞内微电极记录从离体灌注犬肺静脉（N = 28）和右心房（N = 5）。结果在28例肺静脉标本中，刺激自主神经可使肺静脉袖状动作电位时程缩短（APD（90）= 160 ± 17 ~ 92 ± 24 ms;< P.01），并使早期后除极的快速放电（782 ± 158 bpm）开始。初始自发搏动的偶联间期为97 ± 26 ins。未能诱导心律失常与未能缩短APD（90）（151 ± 18至142 ± 8 ms; P = .39）相关。毒蕈碱受体阻断剂（阿托品：3.2 × 10（-8）M）阻止了8/8份制备物中的APD 90缩短，抑制了6/8份制备物中的放电，而β（1）-肾上腺素能受体阻断剂（阿替洛尔：3.2 × 10（-8）M）抑制了8/8份制备物中的放电。用ryanodine（10（-5）M）抑制Ca瞬变完全抑制了6/6个制备物的放电。通过[Ca+2]（o）的瞬时增加抑制正向Na/Ca交换完全抑制了6个制备物中的4个的放电。相同的刺激列车产生阿托品抑制APD（90）缩短灌流右心房游离壁，但未能产生触发arrhythm.CONCLUSIONS的数据表明触发射击犬肺静脉与副交感神经和交感神经联合刺激。钙瞬变增强和Na/Ca交换增加可能是海马形成所必需的。
BACKGROUND Rapid firing within pulmonary vein sleeves frequently initiates atrial fibrillation. The role of the autonomic nervous system in facilitating spontaneous firing is unknown.OBJECTIVES The purpose of this study was to determine if autonomic nerve stimulation within canine atrium and pulmonary vein sleeves initiates arrhythmia formation.METHODS Extracellular bipolar and intracellular microelectrode recordings were obtained from isolated superfused canine pulmonary veins (N = 28) and right atrium (N = 5) during local autonomic nerve stimulation.RESULTS Autonomic nerve stimulation decreased pulmonary vein sleeve action potential duration (APD(90) = 160 ± 17 to 92 ± 24 ms; P < .01) and initiated rapid (782 ± 158 bpm) firing from early afterdepolarizations in 22 of 28 pulmonary vein preparations. The initial spontaneous beat had a coupling interval of 97 26 ins. Failure to induce arrhythmia was associated with a failure to shorten APD(90) (151 ± 18 to 142 ± 8 ms; P = .39). Muscarinic receptor blockade (atropine: 3.2 x 10(-8) M) prevented APD90 shortening in 8 of 8 preparations and suppressed firing in 6 of 8 preparations, whereas β(1)-adrenergic receptor blockade (atenolol: 3.2 x 10(-8) M) suppressed firing in 8 of 8 preparations. Suppression of the Ca transient with ryanodine (10(-5) M) completely suppressed firing in 6 of 6 preparations. Inhibition of forward Na/Ca exchange by a transient increase in [Ca+2](o) completely suppressed firing in 4 of 6 preparations. The same stimulus trains produce atropine-suppressed APD(90) shortening in superfused right atrial free wall but fail to produce triggered arrhythmia.CONCLUSIONS The data demonstrate triggered firing within canine pulmonary veins with combined parasympathetic and sympathetic nerve stimulation. Both an enhanced Ca transient and increased Na/Ca exchange may be required for arrhythima formation.