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首页> 外文期刊>Circulation journal >Altered action potential dynamics in electrically remodeled canine atria: evidence for altered intracellular Ca2+ handling.
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Altered action potential dynamics in electrically remodeled canine atria: evidence for altered intracellular Ca2+ handling.

机译：电重构犬的心房中动作电位动力学的改变：细胞内Ca2 +处理改变的证据。

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BACKGROUND: Electrical instability following sustained rapid excitation has been attributed to altered ion channels. Alterations of Ca(2+) handling could also contribute to abnormal dynamics of action potential, favoring the initiation and perpetuation of arrhythmia. METHODS AND RESULTS: Transmembrane action potentials and twitch force (TF) were recorded from normal (n=6) and remodeled (6-week atrial pacing at 400 beats/min, n=6) canine atria. When the cycle length (CL) was suddenly prolonged in normal atria, both TF and action potential duration (APD) increased on the first beat, and decreased subsequently. Opposite changes were observed with sudden CL shortening. These dynamics in both APD and TF were abolished by ryanodine, but augmented by cyclopiazonic acid, an inhibitor of the sarcoplasmic reticulum (SR) Ca(2+) pump. In remodeled atria (RA), dynamic changes in APD were also concordant with dynamic changes in TF. The transient increases in APD and TF were enhanced, and the transient decreases werereduced compared to normal atria. The maximal slopes of APD and TF restitution curves were flatter and the magnitude of alternans was reduced in RA. The protein expression of SR Ca(2+) ATPase and SR Ca(2+)-release channel in RA was significantly reduced. CONCLUSION: Altered Ca(2+) handling may underlie abnormal APD dynamics in RA.
机译：背景：持续快速激发后的电不稳定性已归因于离子通道的改变。 Ca（2+）处理的改变也可能导致动作电位的异常动态，有利于心律失常的发生和持续。方法和结果：记录正常（n = 6）和重塑（以400次/ min，6周的心房起搏，n = 6）犬心房的跨膜动作电位和抽搐力（TF）。当正常心房中的周期长度（CL）突然延长时，TF和动作电位持续时间（APD）都在第一次搏动时增加，随后减小。突然的CL缩短则观察到相反的变化。 ryanodine废除了APD和TF中的这些动态，但被环质网酸（SR）Ca（2+）泵的抑制剂环吡嗪酸增强。在重塑心房（RA）中，APD的动态变化也与TF的动态变化一致。与正常心房相比，APD和TF的瞬时增加得到增强，并且瞬时减少减少。在RA中，APD和TF恢复曲线的最大斜率较为平坦，而交替RNA的幅度降低了。 SR Ca（2+）ATPase和SR Ca（2 +）-释放通道在RA中的蛋白表达显着降低。结论：改变Ca（2+）处理可能是RA中异常APD动态的基础。

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