Mechano-electric feedback in right atrium after left ventricular infarction in rats
Mechano-electric feedback in right atrium after left ventricular infarction in rats
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DOI：
10.1006/jmcc.1999.1091
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发表时间：
2000-03-01
影响因子：
5
通讯作者：
Lab, MJ
中科院分区：
文献类型：
--
作者：
Kamkin, A;Kiseleva, I;Lab, MJ
左心室心肌梗死（MI）可导致血流动力学负荷条件的改变，从而诱导与心肌细胞表型调节、电异常、节律紊乱和房颤相关的右心房肥大和扩张。然而，关于这些事件的电生理学基础的信息有限。我们研究了在慢性MI的情况下心房牵张是否通过“机械-电反馈”调节心肌细胞的电生理特性，提供了心室梗死后房性心律失常的机制。在左心室MI（n=37）后5周，使用电流钳方案测量右心房组织制备物中的动作电位（AP），并与假手术大鼠（SO. n=10）。在ImN的预负荷下记录收缩活动，并通过测微计施加持续拉伸。在SO中，1.75mN的牵张使复极缩短50%，延长90%。在MI中，机械诱导的电改变在显著低于SO（0.19 mN）的牵拉水平下观察到。心肌梗死后持续牵张延长了90%复极化时的AP，导致牵张激活的去极化（SAD）接近90%复极化（SAD 90）。当达到早发性AP阈值时，在某些准备中观察到类似于心房颤动的电现象。此外，我们观察到在25%、50%和90%复极化时持续时间延长的AP，其中牵拉诱导的SAD接近50%。钆使用的浓度，以抑制拉伸激活通道（40 μ M）抑制机械诱导的电事件。总之，心肌梗死后机械牵张的敏感性增加可能使心房心肌细胞易发生心律失常。这些机械-电改变对钆敏感，表明牵张激活离子通道的参与。(C)北京大学出版社.
Left ventricular myocardial infarction (MI) can lead to alterations in hemodynamic load conditions, thereby inducing right atrial hypertrophy and dilatation associated with phenotypic modulation of cardiomyocytes, electrical abnormalities, rhythm disturbances, and atrial fibrillation. However, there is limited information on the electrophysiological basis for these events. We investigated whether atrial stretch in the setting of chronic MI modulates the electrophysiological properties of cardiomyocytes via "mechano-electric feedback", providing a mechanism for atrial arrhythmia after ventricular infarction, Five weeks after left ventricular MI (n=37), action potentials (AP) were measured in right atrial tissue preparations using a current clamp scheme, and compared to sham-operated rats (SO. n=10). Contractile activity was recorded at a preload of 1 mN, and sustained stretch was applied via a micrometer. In SO, stretch of 1.75 mN shortened repolarization at 50% and prolonged it at 90%. Tn MI, mechanically-induced electrical alterations were observed at a significantly lower Level of stretch than in SO (0.19 mN). Sustained stretch in MI prolonged AP at 90% repolarization giving rise to stretch-activated depolarizations (SAD) near 90% repolarization (SAD90). When reaching threshold for premature APs, electrical phenomena similar to atrial fibrillations were seen in some preparations. Moreover, we observed APs with prolonged duration at 25%, 50%, and 90% repolarization where stretch induced SAD near 50%. Gadolinium used at a concentration to inhibit stretch-activated channels (40 mu M) suppressed mechanically-induced electrical events. In conclusion, increased susceptibility after MI to mechanical stretch may predispose atrial cardiomyocytes to arrhythmia. These mechano-electrical alterations are sensitive to gadolinium suggesting involvement of stretch-activated ion channels.(C) 2000 Academic Press.