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首页> 外文期刊>Journal of Molecular and Cellular Cardiology >Electrophysiology of rabbit ventricular myocytes following sustained rapid ventricular pacing.
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Electrophysiology of rabbit ventricular myocytes following sustained rapid ventricular pacing.

机译：持续快速心室起搏后兔心室肌细胞的电生理。

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摘要

The present study examined changes in electrophysiological properties of ventricular myocytes isolated from rabbit hearts after 2-3 weeks of rapid ventricular pacing. Left ventricular end-diastolic pressure at completion of the pacing period was nearly four-fold greater than in age-matched controls, although there was no significant change in heart weight/body weight ratio. Action potentials recorded in current-clamp mode at low stimulation frequencies were significantly longer in duration and phase 1 diminished in isolated myocytes from paced hearts compared with control. In voltage-clamp experiments. L-type Ca2+ current (ICa) density was not different between groups of myocytes, but the maximum current (at + 10 mV) elicited by 10 microM isoproterenol was approximately 40% less in myocytes from paced hearts. In contrast, maximum ICa elicited by 10 microM forskolin was similar in both groups. The 4-aminopyridine-sensitive transient outward current (Ito) was 65% less (at + 60 mV) in myocytes from paced hearts than from control. However, after approximately 24 h in culture, Ito density in these myocytes returned toward control values. Despite marked reduction in Ito density, the inward rectifier current (IK1) was not different between groups. These data demonstrate that Ito is significantly and reversibly decreased in myocytes from rapidly paced hearts, which may partly account for marked changes in action potential morphology. Although basal ICa was not altered in this group of myocytes compared with control, its modulation by beta-agonists was markedly blunted, probably through a decrease in receptor density or coupling to adenylyl cyclase. These changes in myocyte K+ and Ca2+ channel behavior in paced hearts may relate to impaired contractility and arrhythmogenesis that is characteristic of the intact failing heart.
机译：本研究检查了快速起搏2-3周后从兔心脏中分离出的心室心肌细胞电生理特性的变化。起搏期结束时左心室舒张末期压力比年龄匹配的对照组高近四倍，尽管心脏重量/体重比没有明显变化。与对照组相比，以电流钳模式在低刺激频率下记录的动作电位的持续时间显着更长，并且从起搏的心脏中分离出的心肌细胞中的1期减少。在电压钳实验中。两组心肌细胞之间的L型Ca2 +电流（ICa）密度没有差异，但10 microM异丙肾上腺素引起的最大电流（约10 mV）比起搏心脏的心肌细胞少约40％。相反，两组中由10 microM福司柯林引起的最大ICa相似。从起搏的心脏中获取的4-氨基吡啶敏感性瞬时外向电流（Ito）比正常人少65％（在+ 60 mV时）。然而，在培养约24小时后，这些肌细胞中的Ito密度恢复到对照值。尽管It​​o密度显着降低，但两组之间的内部整流器电流（IK1）并无不同。这些数据表明，来自快速起搏的心脏的心肌细胞中Ito显着且可逆地降低，这可能部分解释了动作电位形态的明显变化。尽管与对照组相比，该组心肌细胞的基础ICa并未改变，但其β激动剂的调节作用明显减弱，可能是由于受体密度降低或与腺苷酸环化酶偶联所致。在起搏的心脏中，心肌细胞K +和Ca2 +通道行为的这些变化可能与收缩力和心律失常有关，这是完整的衰竭心脏的特征。

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